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OSCC Flashcards

1
Q

Where does the word “tumour” originate from?

A

latin - swelling

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2
Q

What is the general nomenclature for benign tumours?

A

-oma to the cell type the neoplasm arises from

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3
Q

What is the exception to the normal rule of naming benign tumours?

A

epithelial neoplasms

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4
Q

How are benign epithelial neoplasms classified?

A

on their microscopic or macroscopic patterns

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5
Q

Adenoma

A

benign gland patterned epithelial neoplasm

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6
Q

Papilloma

A

benign epithelial neoplasm producing microscopic or macroscopic fingerlike fronds

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7
Q

How are malignant epithelial origin neoplasms named?

A

-carcinoma

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8
Q

How are malignant CT neoplasms named?

A

-sarcoma

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9
Q

How are malignant epithelial neoplasms classified?

A

on their microscopic or macroscopic pattern

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10
Q

What do the neoplastic cells resemble in squamous cell carcinoma?

A

stratified squamous epithelium

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11
Q

What are the three exceptions in malignant nomenclature?

A

lymphoma, mesothelioma, melanoma

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12
Q

Growth type of benign tumours

A

expansive

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13
Q

Growth type of malignant tumours

A

infiltrating

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14
Q

Growth speed of benign tumours

A

usually slow

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15
Q

Growth speed of malignant tumours

A

usually rapid

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16
Q

Do benign tumours often stabilise?

A

yes

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17
Q

Do malignant tumours often stabilise?

A

no it would be exceptional

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18
Q

Structure of benign tumours

A

typical

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19
Q

Structure of malignant tumours

A

atypical (dedifferentiation - anaplasia)

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20
Q

Mitoses in benign tumours

A

rare and typical

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21
Q

Mitoses in malignant tumours

A

numerous and atypical

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22
Q

Evolution of benign tumours

A

local

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23
Q

Evolution of malignant tumours

A

local and general

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24
Q

Local consequences of benign tumours

A

variable - compressions

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25
Q

3 local severe consequences of malignant tumours

A

infiltration, destruction, necrosis

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26
Q

General consequences of benign tumours

A

none unless secretory tumours/particular sites

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27
Q

In what phase are the general consequences of malignant tumours constant and severe?

A

generalisation phase

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28
Q

Which type of tumour is always fatal without treatment?

A

malignant

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29
Q

Do benign tumours tend to recur?

A

no

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30
Q

OSCC gender ratio

A

M 2.22:1 F

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31
Q

Three most common oral cancers

A

OSCC, NHL, mucoepidermoid carcinoma

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32
Q

Which continent has a high prevalence of oral cancer?

A

Asia

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33
Q

Black patients and oral cancer

A

detected later and greater mortality

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34
Q

what percentage of cancers are oral?

A

2%

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35
Q

what % of oral cancer is in over 55s?

A

78%

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36
Q

Most common oral cancer site

A

tonsils

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37
Q

2nd most common oral cancer site

A

tongue

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38
Q

3rd most common oral cancer site

A

base of tongue

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39
Q

where does OSCC originate from?

A

oral keratinocytes

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40
Q

what % of oral cancers are SCC?

A

over 90%

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41
Q

3 most common sites for OSCC?

A

tongue, FOM, gingiva

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42
Q

In countries where betel quid chewing is practiced, where are the 2 most common OSCC sites?

A

buccal mucosa and gingiva

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43
Q

How is early stage OSCC usually detected and why?

A

incidentally as tends to be asymptomatic

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44
Q

What are the 8 subtypes of OSCC?

A
  1. verrucous carcinoma
  2. basal SCC
  3. papillary SCC
  4. spindle cell SCC
  5. Adenosquamous carcinoma
  6. lymph-epithelial carcinoma
  7. acantholytic SCC
  8. carcinoma cuniculatum
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45
Q

Which subtypes of OSCC have a better prognosis?

A

verrucous carcinoma

papillary SCC

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46
Q

which subtypes of OSCC have a worse prognosis?

A

spindle cell SCC

adenosquamous carcinoma

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47
Q

which 3 subtypes have an exophytic verruco-papillary component?

A

verrucous carcinoma
carcinoma cuniculatum
papillary SCC

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48
Q

What are the 4 clinical appearances of OSCC?

A

OPMDs
ulceration
speckled
exophytic growth

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49
Q

OSCC appearance - OPMDs

A

flat/slightly raised red/white/mixed exophytic lesions

may get changes in surface texture (smooth, granular, rough, crusted)

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50
Q

OSCC appearance - ulceration

A

solitary lesion that is not healing/responding to conservative management
usually presents with irregular and indurated margins

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51
Q

OSCC appearance - speckled

A

ill-defined mixed white-red lesions with granular aspects

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52
Q

OSCC appearance - exophytic growth

A

irregular overgrowth with a smooth or verrucopapillary (verrucous carcinoma) surface above normal mucosa

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53
Q

Late stage OSCC - what is the usual cause of pain?

A

ulceration

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54
Q

Late stage OSCC - what leads to trismus?

A

OSCC of buccal mucosa and involvement of the infra temporal fossa

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55
Q

Late stage OSCC - FOM symptoms

A

restriction of tongue mobility
progressive difficulty in mastication and speech
drooling of saliva

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56
Q

Late stage OSCC - gingiva

A

excessive mobility of involved teeth due to involvement of periosteum and possible spread to bone

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57
Q

Late stage OSCC - tongue base

A 
sensation of fullness in throat
dysphagia
sensation of a lump in neck/throat
voice changes
ear pain
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58
Q

What 3 parts of the diagnostic pathway do you need for staging and grading?

A

pt history and exam
histopathology and clinical adjuncts
radiologic imaging

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59
Q

2 predictors of prognosis

A

staging and grading

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60
Q

Grading

A

cytologic differentiation of the cells - how much the cancer cells look like healthy cells under a microscope

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61
Q

Staging

A

where has the cancer spread?

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62
Q

5 morphologic features considered in grading

A 
degree of keratinisation
nuclear polymorphism
number of mitoses
pattern of invasion
host response
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63
Q

Which morphologic feature is excluded from the Bryne grading system?

A

number of mitoses

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64
Q

what is the ideal pattern of invasion of a tumour?

A

pushing, well-delineated, infiltrating borders

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65
Q

Grade X

A

differentiation can’t be assessed

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66
Q

Grade 1

A

well-differentiated

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67
Q

Grade 2

A

moderately differentiated

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68
Q

Grade 3

A

poorly differentiated

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69
Q

Grade 4

A

undifferentiated or anaplastic

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70
Q

Grades

A

X, 1, 2, 3, 4

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71
Q

What does a lower grade mean?

A

better prognosis

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72
Q

What does the grade predict?

A

how quickly the cancer will spread

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73
Q

What does TNM staging stand for?

A

Tumour, Node, Metastasis

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74
Q

TNM staging - T stages

A

T0-4

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75
Q

TNM staging - what does T describe?

A

size (cm) and location, how much the tumour has grown into nearby tissues

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76
Q

TNM staging - N stages

A

N0-3

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77
Q

TNM staging - what does N describe?

A

whether the cancer has spread to lymph nodes - regional or distant

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78
Q

TNM staging - M stages

A

M0 or M1

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79
Q

TNM staging - what does M describe?

A

whether cancer has spread to other parts of the body - distant metastasis

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80
Q

What does the 8th edition cancer staging not include?

A

non-epithelial tumours

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81
Q

what does T incorporate in 8th edition cancer staging?

A

DOI

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82
Q

what does N incorporate in 8th edition cancer staging?

A

ENE

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83
Q

Tumour Thickness

A

mucosal surface of tumour to deepest point of tissue invasion in a perpendicular fashion

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84
Q

Depth of Invasion

A

level of basement membrane adjacent to normal mucosa to deepest point of tumour invasion

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85
Q

What DOI is associated with a significantly increased risk of recurrence and nodal metastasis?

A

> 10mm

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86
Q

When should elective neck dissection be considered?

A

for tumours <5mm deep

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87
Q

ENE

A

extension of metastatic cells through the nodal capsule into the perinodal tissue

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88
Q

what is the advantage of 8th edition cancer staging?

A

leads to identification if OSCC pts with a worse prognosis who might benefit from an improved post-op tx strategy

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89
Q

give some examples of where oral cancer can metastasise to

A

anywhere - lung, heart, vertebra, chest wall

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90
Q

What do you do before an imaging assessment?

A

establish the primary site and any neck metastasis clinically
have histological diagnosis

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91
Q

What is the role of radiology?

A

accurately stage the full extent and distant spread of disease with TNM system

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92
Q

What are the focus areas for imaging?

A

local extent of primary tumour
spread to loco regional cervical lymph nodes
detection of metastatic disease precluding cure and synchronous primary tumours of lung/upper aero-digestive tract

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93
Q

What is the main form of imaging used to detect the primary tumour?

A

CT

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94
Q

what is CT used for?

A

detecting primary tumour

local bone infiltration

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95
Q

multi-detector CT (MDCT)

A

precisely determine boundaries of tumour

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96
Q

contrast-enhanced CT (CECT)

A

accurately determine LN metastases

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97
Q

what can’t CT differentiate between?

A

recurrences, surgical scars and adverse reactions after radiation therapy

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98
Q

Give a form of imaging using ionising radiation

A

CT

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99
Q

give 2 examples of imaging without ionising radiation

A

MRI, US

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100
Q

give a form of functional imaging

A

Positron Emission Tomography combined with CT (PET-CT)

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101
Q

what can MRI determine the involvement of?

A

local STs, bone marrow, bones, vessels, nerves

local LN and distant metastases

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102
Q

what is MRI better than CT/CBCT for?

A

assessment of STs

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103
Q

2 advantages of US

A

cheap and non-invasive

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104
Q

3 uses of US

A

evaluate superficial lesions
evaluate LNs
guide FNAB

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105
Q

what can colour doppler US be used for and what is the advantage of this?

A

to determine the type of blood vascularity in a lesion

often increases the specificity of diagnosis

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106
Q

what is the advantage of PET-CT over CT or MRI?

A

may detect malignancy in structures which appear normal or are difficult to assess on CT/MRI e.g. small vol LN metastases

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107
Q

give 3 uses of PET-CT

A

look for the primary tumour site when metastases are found earlier (CUP)
detect recurrence of primary tumours
detect distant metastases of primary tumours

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108
Q

when is PET-CT recommended?

A

advanced cancer stages

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109
Q

8th edition cancer staging - 4 subsections

A

definition of primary tumour (T)
definition of regional LN (N, pN)
definition of regional LN (N, cN)
definition of distant metastases (M)

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110
Q

8th edition cancer staging - T stages

A 
TX
Tis
T1
T2
T3
T4a
T4b
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111
Q

8th edition cancer staging - TX

A

primary tumour can’t be assessed

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112
Q

8th edition cancer staging - Tis

A

carcinoma in situ

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113
Q

8th edition cancer staging - T1

A

< or = 2cm

DOI < or = 5mm

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114
Q

8th edition cancer staging - T2

A

25mm

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115
Q

8th edition cancer staging - T3

A

210mm
OR
>4cm, DOI <=10mm

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116
Q

8th edition cancer staging - T4a

A

moderately advanced local disease
>4cm, DOI >10mm
OR
invaded adjacent structures only (superficial erosion of bone/socket alone by a gingival primary is not T4)

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117
Q

8th edition cancer staging - T4b

A

v advanced local disease - tumour invades masticator space, pterygoid plates, or skull base and/or encases ICA

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118
Q

8th edition cancer staging - NX

A

regional lymph nodes can’t be assessed

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119
Q

8th edition cancer staging - N0

A

no regional LN metastasis

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120
Q

8th edition cancer staging - N1

A

1 ipsilateral
<=3cm
ENE -

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121
Q

8th edition cancer staging - N2a

A

single ipsilateral, 3

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122
Q

8th edition cancer staging - N2b

A

multiple ipsilateral <=6cm, ENE -

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123
Q

8th edition cancer staging - N2c

A

bilateral/contralateral, <=6cm, ENE -

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124
Q

8th edition cancer staging - N3a

A

> 6cm, ENE -

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125
Q

8th edition cancer staging - N3b

A

any nodes and clinically overt ENE+

OR pN3b:
1 ipsilateral >3cm, ENE+
or
multiple ipsilateral/contralateral/bilateral ENE+
or
single contralateral, any size, ENE+
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126
Q

8th edition cancer staging - cM0

A

no distant metastasis

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127
Q

8th edition cancer staging - cM1

A

distant metastasis

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128
Q

8th edition cancer staging - pM1

A

distant metastasis, microscopically confirmed

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129
Q

8th edition cancer staging - what does U or L for N category mean?

A

indicates metastasis above the lower border of the cricoid (U) or below (L)

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130
Q

8th edition cancer staging - prognostic staging groups

A 
0
1
2
3
4a
4b
4c
131
Q

8th edition cancer staging - stage 0

132
Q

8th edition cancer staging - stage 1

133
Q

8th edition cancer staging - stage 2

134
Q

8th edition cancer staging - stage 3

A

T3 N0 M0
or
T1/2/3 N1 M0

135
Q

8th edition cancer staging - stage 4a

A

T4a N0/1 M0
or
T1/2/3/4a N2 M0

136
Q

8th edition cancer staging - stage 4b

A

any T N3 M0
or
T4b any N M0

137
Q

8th edition cancer staging - stage 4c

A

any T
any N
M1

138
Q

how do involved LNs initially present?

A

soft
mobile
non-tender

139
Q

how do involved LNs present at the advanced stage or in aggressive disease?

A

enlarged
firm/hard texture
usually non-tender fixation to adjacent tissue due to invasion of cells through the capsule

140
Q

Lymph node levels

A 
1a
1b
2a
2b
3
4
5a
5b
6
7
141
Q

LN level 1a

142
Q

LN level 1b

A

submandibular

143
Q

LN level 2a and b

A

upper jugular

144
Q

LN level 3

A

mid jugular

145
Q

LN level 4

A

lower jugular

146
Q

LN level 5a and b

A

posterior triangle

147
Q

LN level 6

A

anterior compartment

148
Q

LN level 7

A

superior mediastinal

149
Q

location of LN level 1a - submental

A

between anterior bodies of digastric muscles and hyoid bone

150
Q

what do the submental (1a) nodes drain?

A

lower lip and chin

secondary drainage for anterior tongue

151
Q

location of LN level 1b - submandibular

A

from U to L margin of submandibular gland
medial to mandible
lateral to posterior body of digastric muscle

152
Q

what do the submandibular (1b) nodes drain?

A

oral cavity
lower nasal cavity
submandibular gland

153
Q

location of LN level 2 - upper jugular

A

from underside of lateral process of C1 to hyoid
medial to SCM
lateral to scalene muscles

154
Q

what is LN level 2 divided into a and b by?

A

posterior border of IJV

155
Q

what do the upper jugular (2) nodes drain?

A 
nasal cavity
nasopharynx
oropharynx
larynx
hypopharynx
parotid gland
secondary drainage for oral cavity
156
Q

location of LN level 3 - mid jugular

A

from bottom of hyoid to bottom of cricoid cartilage
medial to SCM
lateral to scalene muscles

157
Q

what do the mid jugular (3) nodes drain?

A 
nasopharynx
oral cavity
oropharynx
larynx
hypopharynx
158
Q

location of LN level 4 - lower jugular

A

from bottom of cricoid to 2cm above sternoclavicular joint
medial to SCM
lateral to scalene muscle

159
Q

what do the lower jugular (4) nodes drain?

A 
hypopharynx
larynx
thyroid
cervical oesophagus
distal drainage from higher cervical levels
160
Q

location of LN level 5 a and b - posterior triangle

A

from hyoid to transverse cervical vessels
medial to tail of SCM
lateral to anterior border of trapezius

161
Q

what do the posterior triangle (5) nodes drain?

A

nasopharynx
oropharynx
thyroid
posterior sack

162
Q

location of LN level 6 - anterior compartment

A

from lower edge of hyoid to upper edge of sternal manubrium

between SCMs

163
Q

what is LN level 6 divided into a and b by?

A

lower margin of cricoid cartilage

164
Q

what does LN level 6 drain?

A 
lower face
tip of tongue
FOM
anterior neck
hypopharynx
thyroid
larynx
cervical oesophagus
165
Q

location of LN level 7 - superior mediastinal

A

from superior edge of manubrium sterni to upper border of arch of aorta
between left CCA and right innominate artery

166
Q

what do the superior mediastinal (7) nodes drain?

A

nasopharynx
soft palate
tonsillar fossa
posterior pharyngeal wall

167
Q

Predominant lymph node levels for metastasis - buccal

168
Q

Predominant lymph node levels for metastasis - gingival

169
Q

Predominant lymph node levels for metastasis - retromolar

A

1b/2a

62-80%

170
Q

Predominant lymph node levels for metastasis - maxillary

A

1b/2a

60-70%

171
Q

Predominant lymph node levels for metastasis - soft palate

A

1/2a (55%)

but also 25% contralateral involvement

172
Q

Predominant lymph node levels for metastasis - tongue

A 
2b 8%
1/2a 75%
4 6-8%
contralateral 6-12%
more posterior = higher chance to involve the upper jugular and contralateral nodal metastasis, due to higher lymphatic interconnections posteriorly towards base of tongue
173
Q

Predominant lymph node levels for metastasis - FOM

A

1/2a 75%

contralateral 8-10%

174
Q

in OSCC pts, when are level 4 (lower jugular) nodes only usually involved?

A

when other neck levels are positive for metastases

175
Q

what feature of the primary tumour gives a greater risk of bilateral cervical node spread?

A

the closer to the midline the primary is

176
Q

which areas does oropharyngeal cancer include?

A 
base of tongue
inferior (anterior) surface of the soft palate and uvula
anterior and posterior tonsillar pillars
pharyngeal tonsils
lateral and posterior pharyngeal walls
177
Q

staging for OPC non-HPV mediated (p16-)

A

same categories for oral and lip SCC

- T, cN, pN, M, prognostic staging group

178
Q

staging for HPV-mediated (p16+) OPC - T stages

A 
T0
T1
T2
T3
T4
179
Q

staging for HPV-mediated (p16+) OPC - T0

A

no primary identified (but identifiable neck node)

180
Q

staging for HPV-mediated (p16+) OPC - T1

181
Q

staging for HPV-mediated (p16+) OPC - T2

182
Q

staging for HPV-mediated (p16+) OPC - T3

A

> 4cm
OR
extension to lingual surface of epiglottis

183
Q

staging for HPV-mediated (p16+) OPC - T4

A

moderately advanced local disease
(tumour invades the larynx, extrinsic tongue muscles, medial pterygoid, hard palate or mandible or beyond (mucosal extension to lingual surface of epiglottis from primary tumours of the base of the tongue and vallecula does not constitute invasion of the larynx))

184
Q

staging for HPV-mediated (p16+) OPC - cN stages

A 
cNX
cN0
cN1
cN2
cN3
185
Q

staging for HPV-mediated (p16+) OPC - cNX

A

regional LNs cannot be assessed

186
Q

staging for HPV-mediated (p16+) OPC - cN0

A

no regional LN metastasis

187
Q

staging for HPV-mediated (p16+) OPC - cN1

A

> = 1 ipsilateral, less than or equal to 6cm

188
Q

staging for HPV-mediated (p16+) OPC - cN2

A

contralateral or bilateral, less than or equal to 6cm

189
Q

staging for HPV-mediated (p16+) OPC - cN2

190
Q

staging for HPV-mediated (p16+) OPC - pN stages

A

pNX
pN0
pN1
pN2

191
Q

staging for HPV-mediated (p16+) OPC - pNX

A

regional LNs cannot be assessed

192
Q

staging for HPV-mediated (p16+) OPC - pN0

A

no regional LN metastasis

193
Q

staging for HPV-mediated (p16+) OPC - pN1

A

less than or equal to 4 LNs

194
Q

staging for HPV-mediated (p16+) OPC - pN2

195
Q

staging for HPV-mediated (p16+) OPC - M stages

196
Q

staging for HPV-mediated (p16+) OPC - cM0

A

no distant metastasis

197
Q

staging for HPV-mediated (p16+) OPC - cM1

A

distant metastasis

198
Q

staging for HPV-mediated (p16+) OPC - pM1

A

distant metastasis, microscopically confirmed

199
Q

staging for HPV-mediated (p16+) OPC - cTNM prognostic staging group 1

A

T0/1/2
N0/1
M0

200
Q

staging for HPV-mediated (p16+) OPC - cTNM prognostic staging group 2

A

T0/1/2. N2. M0
or
T3. N0/1/2. M0

201
Q

staging for HPV-mediated (p16+) OPC - cTNM prognostic staging group 3

A

any T. N3. M0
or
T4. N0/1/2/3. M0

202
Q

staging for HPV-mediated (p16+) OPC - cTNM prognostic staging group 4

A

any T
any N
M1

203
Q

staging for HPV-mediated (p16+) OPC - pTNM prognostic staging group 1

A

T0/1/2
N0/1
M0

204
Q

staging for HPV-mediated (p16+) OPC - pTNM prognostic staging group 2

A

T0/1/2. N2. M0
or
T3/4. N0/1. M0

205
Q

staging for HPV-mediated (p16+) OPC - pTNM prognostic staging group 3

206
Q

staging for HPV-mediated (p16+) OPC - pTNM prognostic staging group 4

A

any T
any N
M1

207
Q

three aspects of multimodal approach to treatment

A

surgery
chemo
radio

208
Q

OSCC stage 1 and 2 tx

A

surgery or radio

209
Q

OSCC stage 3 and 4 tx

A

concomitant radio/chemo (+surgery) better outcomes than radio (+surgery)

210
Q

what are definitive radio, concurrent CRT and sequential therapy usually limited to?

A

pts who are

  • medically inoperable
  • unresectable disease
  • resectable disease where surgical resection cannot be accomplished with acceptable long-term functional consequences
211
Q

what is the goal of surgery?

A

completely resect the primary tumour and any neck deposit, wherever achievable, to prevent recurrence and conserve high survival rate

212
Q

why is surgery preferred over radio for stage 1/2?

A

reduced morbidity

213
Q

stage 3/4 surgery

A

complete resection of primary tumour and neck nodes

214
Q

why is it important to ensure negative resection margins?

A

increased risk of treatment failure in patients with positive surgical margins

215
Q

how do you check for negative margins?

A

specimen examined and microscopic margins checked

216
Q

give 3 examples of surgical techniques

A

open resection
transoral robotic surgery (TORS)
transoral laser microsurgery (TLM)

217
Q

give 2 contraindications to open resection

A

T4b - invasion of the masticator space, pterygoid plates, skull base or carotid encasement
pt perception of QOL

218
Q

what is the reason behind using minimally invasive surgery: TORS, TLM?

A

it mat provide improved functional outcomes with minimal surgical morbidity and enhance the pathologic staging

219
Q

how does TORS work?

A

surgeon distant from patient controlling robotic unit

220
Q

indications for minimally invasive surgery

A

T1-2 tumours of oropharynx but only if surgeon has good oral access

221
Q

contraindications for minimally invasive surgery

A

retrognathia
class 2 malocclusion
limited cervical extension
SP tumour - higher rate of rhinolalia, velopharyngeal insufficiency and nasopharyngeal reflux

222
Q

advantages of minimally invasive surgery

A 
no external incision
no mandibulotomy or transmandibular access
decreased immediate post-op toxicity
shorter post-op hospitalisation time
faster fct recovery
enhanced visualisation - 3D+magnification of the field
elimination of physiologic tremors
movements can be scaled
fatigue reduction
training - teaching purposes
223
Q

disadvantages of minimally invasive surgery

A

absence of tactile sensation - unable to feel tissue resistance or how tight a knot is
equipment size and weight
£££ - installation and annual maintenance

224
Q

give the 4 types of neck dissection

A

comprehensive
selective
superselective
elective

225
Q

comprehensive neck dissection

A

all LN levels of the neck are removed with/without 3 non-lymphatic structures (SCM, IJV, CN12)

226
Q

selective neck dissection

A

not all LN levels are dissected
OSCC at least level 1-3
oropharyngeal SCC at least level 2-4

227
Q

superselective neck dissection

A

dissection of only one or two contiguous LN levels to further decrease the morbidity of neck dissection

228
Q

elective neck dissection

A

dissection of the appropriate nodal level, based on the risk of occult microscopic metastases

229
Q

for OSCC what do you use to predict occult metastasis and guide neck dissection decision?

A

SLNB or DOI

230
Q

what DOI is an accurate cut off value for performing an elective neck dissection in early stage OSCC?

A

DOI more than or equal to 4mm

231
Q

what is a SLNB?

A

identifying and harvesting the initial node to which the primary tumour drains
high diagnostic accuracy

232
Q

indications for a SLNB

A

to assess pts with biopsy-proven OSCC staged as early tumours with clinically (palpation) and radiologically (US, CT, MRI) N0 neck
assess bilateral N0 necks in primary tumours close to or crossing the midline

233
Q

what can improve SLNB diagnostic sensitivity?

A

using immunohistochemistry

234
Q

how does radiation therapy work?

A

uses high energy ionising radiation to disrupt the integrity of malignant cells through focal DNA damage, while doing as little harm as possible to normal cells

235
Q

4 uses of radiation therapy

A

exclusive treatment of primary cancer
adjuvant therapy after surgery
adjuvant therapy before surgery
palliative therapy

236
Q

radio - exclusive treatment of primary cancer

A

early stage cancer

unresectable/advanced in combination with chemo

237
Q

radio - adjuvant therapy after surgery

A

+/- chemo to control positive neck nodes and/or killing remaining cancer cells in + margins

238
Q

radio - adjuvant therapy before surgery

A

+/- chemo to shrink size of tumour

239
Q

radio - palliative therapy

A

to control symptoms of advanced OSCC e.g. pain, bleeding, dysphagia, and problems caused by bone metastases, and to give pt a better QOL

240
Q

types of radiotherapy

A

external beam radiotherapy

(internal) brachytherapy

241
Q

how does EBRT work?

A

machine used to aim high energy rays/beams from outside the body into the tumour
focus the radiation on the exact location it needs to be, so normal tissues are affected as little as possible

242
Q

normal treatment regime for EBRT

A

5 days a week for 6-7wks

243
Q

2 examples of other EBRT schedules and their + and - s

A

hyperfractionation
accelerated fractionation
+may reduce the risk of cancer coming back in or near the place it started (local recurrence)
-tend to have more severe side effects

244
Q

EBRT - hyperfractionation

A

total radiation dose in a larger number of doses e.g. 2 smaller doses per day

245
Q

EBRT - accelerated fractionation

A

> or= 2 doses given each day so treatment completed faster

246
Q

what is EBRT simulation technique for?

A

determine areas that will be radiated through a simulator

247
Q

EBRT simulation technique procedure

A

supine on table, arms at sides, neck extended
immobilised by a thermoplastic head/shoulders mask to secure and gently hold head in place
head in neutral position
don’t swallow during scanning
scan to identify target volumes
mark pt with tattoos in tx fields so they can be set up each day with precision, while allowing pt to wash without obscuring tx fields

248
Q

name some types of EBRT

A 
intensity modulated (IMRT)
3D conformal RT (3D-CRT)
image guided (IGRT)
volumetric modulated arc therapy (VMAT/Rapid arc)
intensity modulated proton therapy (IMPT)
stereotactic radio surgery (SRS)
stereotactic body RT (SBRT)
intraoperative RT (IORT)
249
Q

what is IMRT?

A

high precision RT that uses computer controlled linear accelerators to deliver precise radiation doses to a malignant tumour or specific areas within the tumour

250
Q

IMRT - what is the dose to target usually proportional to?

A

estimated tumour burden

251
Q

advantages of IMRT

A

higher doses to be focused on the tumour
spares organs at risk (OAR)

(more individualised tx)

252
Q

internal radiation therapy (brachytherapy)

A

hollow catheters placed into/around the tumour during surgery
left in place for several days while pt stays in hospital
radioactive materials are put into tubes for a short time each day
small radioactive pellets (rice) put right into tumour. give off low levels of radioactivity for several weeks and over time lose their strength
pellets just left in place and rarely cause any problems

253
Q

when do short term RT side effects occur?

A

visible during/immediately after RT and may last for 2-3weeks after tx

254
Q

short term RT side effects

A 
oral mucositis
dental pain
taste loss
trismus (due to pain)
odynophagia
dysphagia
candidiasis
radiation dermatitis (RD)
ORN
255
Q

when do long term RT side effects occur?

A

visible several weeks after RT and may last for long time or even permanently after tx

256
Q

long term RT side effects

A

salivary gland hypofct
trismus (muscle fibrosis)
extensive dentition breakdown due to radiation caries (RC)
ORN (can develop over months or years after completion of RT)

257
Q

what is ORN?

A

irradiated bone becomes devitalised and exposed through the overlying skin or mucosa without healing for 3m, without recurrences of tumour

258
Q

why is the mandible more affected by ORN?

A

only supplied by inferior alveolar artery, whereas maxilla supplied by anterior, middle and posterior superior alveolar arteries

259
Q

ORN staging classification

A 
no universally used one
Marx
Epstein et al
Schwartz and Kagan
Notani et al
260
Q

what % of ORN cases develop within the first 3 years after radiotherapy?

261
Q

risk factors for ORN

A

hyperfractionated irradiation regimen
high total dose (6000-7000cGy)
literature suggests chemo and radio increases incidence
pre-irradiation and post-irradiation dental extractions
poor OH and PDD
tobacco and alcohol use

262
Q

ORN conservative tx

A 
improve OH
antibiotics
minimal surgical debridement
hyperbaric 02 therapy
medical management: pentoxifylline, tocopherol
263
Q

ORN surgical tx

A

sequestrectomy
saucerisation
segmental resection and free flap reconstruction

264
Q

what is chemotherapy?

A

a drug tx to kill fast growing cancer cells that multiply much more quickly than most cells in the body

265
Q

indications for chemotherapy

A
  1. can use as the primary or sole tx for cancer
  2. adjuvant therapy after surgery (+/- radio) to kill any residual cancer cells
  3. adjuvant therapy before surgery (+/-radio) to shrink the size of the tumour
  4. palliative therapy to relieve S+S of advanced OSCC and give pt a better QOL
266
Q

which gender may benefit more from chemo in CST?

267
Q

3 types of chemotherapy

A

adjuvant
induction
concomitant

268
Q

adjuvant chemo

A

given after surgery for reducing the incidence of distant metastatic recurrence

269
Q

induction chemo

A

given before definitive tx (radio/surgery)

potentially reduce the risk of distant metastasis and the size of the primary tumour to improve loco regional control

270
Q

concomitant chemo

A

given with surgery/radio to achieve radiosensitisation

271
Q

give 2 indications for adjuvant chemotherapy

A

locally advanced disease HNSCC (stage 3-4b)

recurrent or metastatic HNSCC (stage 4c)

272
Q

adjuvant chemo for locally advanced stage 3-4b

A

platinum based chemo and radio

- cisplatin, paclitaxel, 5-fluorouracil, carboplatin, cetuximab

273
Q

adjuvant chemo for recurrent or metastatic stage 4c

A

cetuximab and platinum based chemo - cisplatin/carboplatin and 5-fluorouracil

or anti PD-1 immunotherapy plus chemo

  • pembrolizumab and platinum and 5-fluorouracil
  • nivolumab/pembrolizumab without chemo if pt has PD-LI+ recurrent or metastatic HNSCC
274
Q

CRT

A

chemo given as a radiation sensitiser with the goal of reducing radiation resistance

275
Q

chemo oral side effects

A 
mucositis
infection
oral lichenoid reactions
hyperpigmentations
hyposalivation
altered taste
bleeding 
MRONJ
SJS/TEN
276
Q

treatment of early stage lip SCC

A 
surgical resection
definitive radio if surgery not feasible/pt unfit for surgery
if deep (esp U lip) consider prophylactic selective neck dissection
277
Q

post-surgical tx of early stage lip SCC

A

+ margins: reresection / radio

primary tumour with perineural/lymphovascular invasion: radio adjuvant

278
Q

treatment of locally advanced lip SCC

A

surgical resection
definitive concurrent radio and chemo if pt unfit for surgery or surgery not feasible
often need neck dissection

279
Q

post-surgical tx of locally advanced lip SCC

A

+ margins: reresection and adjuvant radio/chemoradio
perineural/vascular/lymphatic invasion: adjuvant radio
ENE: adjuvant chemo radio

280
Q

treatment of early stage oral cavity SCC

A

resection
definitive radio if surgery not feasible - consider conformed techniques and brachytherapy

neck dissection depends on site, extent and thickness
- SLNB for DOI >3mm and most stage 2 lesions

281
Q

post-op adjuvant therapy for early and locally advanced stage oral cavity SCC

A

1+ LN - discuss radio
ENE - systemic therapy and radio
close or + margin - reresection/ (radio); tx with concurrent chemo radio
invasion - consider radio

282
Q

treatment of locally advanced stage oral cavity SCC

A

resection
definitive concurrent radio and chemo radio if can’t do surgery
ipsilateral/bilateral neck dissection
- if LNs involved, inc neck radio

283
Q

treatment of early stage oropharyngeal SCC

A

clinical trials
definitive radio
surgical resection of primary tumour - minimally invasive techniques
consider elective nodal therapy

284
Q

early stage and locally advanced oropharyngeal SCC post-op adjuvant therapy

A

CRT

if positive margins reresection then radio

285
Q

treatment of locally advanced stage oropharyngeal SCC

A

concurrent CRT
resection (but usually reserved for smaller primary tumours)
radio for neck +/- dissection

286
Q

risk factors for oral cancer

A

predisposing factors
genetic susceptibility
OPMDs
oral microbiome

287
Q

predisposing factors for oral cancer

A

social - alcohol and tobacco (smoked and smokeless)
diet - low fruit and veg
physical agents - UV light, radiation
chemicals - env and occupational exposures (arsenic, benzene, asbestos)

288
Q

what effect do combined predisposing factors have?

A

synergistic effect

289
Q

give a way in which alcohol causes cancer

A

ethanol—ADH—>acetaldehyde—ALDH—>acetate(energy)
if too much alcohol drunk, body can’t process it fast enough so get build up of acetaldehyde - toxic and causes DNA damage

290
Q

what infection in men may high alcohol lead to an increased risk of?

A

prevalent HPV infections

291
Q

which foods may decrease the risk of oral cancer?

A

fruit and veg

fish and omega 3 fatty acids

292
Q

which foods may increase the risk of oral cancer?

A

high consumption of processed meat

293
Q

is there a significant association between total/red/white meat and risk of oral cancer?

294
Q

do dietary supplements have the same effect on risk reduction of cancer as foods?

295
Q

oral hygiene as a risk factor for oral cancer

A

may also be a prognostic factor
aids the carcinogenic potential of other known carcinogens e.g. tobacco and alcohol
- increases carcinogenicity of known carcinogens

296
Q

oral microbiome as a risk factor for oral cancer

A

candida associated with increased risk

HPV

297
Q

HPV manifestations

A

benign anogenital and cutaneous warts
respiratory papillomatosis
oral lesions

298
Q

oral HPV manifestations

A

verruca - verruca vulgaris or common wart
condyloma - condyloma acuminatum
papilloma

not OPMDs

299
Q

HPV genome structure - what 2 regions is it divided into?

A

E - early

L - late

300
Q

HPV genome structure - E region

A

45% of viral genome
encodes the proteins that are produced initially
E1,2,4,5,6,7 open reading frames

301
Q

HPV genome structure - L region

A

40% of viral genome
encodes the proteins that are produced after synthesis of the proteins of the E region
L1,2 open reading frames

302
Q

HPV genome structure - non-coding/designated long control (LCR) / upstream regulatory (URR) region

A

15% of viral genome

involved in the control of viral gene expression

303
Q

HPV genome structure - role of E proteins

A

destructs/inactivates TS protein
viral DNA replication
assembly and release of the viral particle
interaction with the epidermal GF

304
Q

HPV genome structure - role of the L proteins

A

capsid protein in the viral particle

305
Q

3 roles of the GDP in oral cancer

A

primary prevention
secondary prevention
overall health care of OSCC pt

306
Q

primary prevention

A

educate pts about oral cancer and its risk factors

307
Q

secondary prevention

A

early detection of OPMDs and OSCC - oral cancer screening

referral if suspicious

308
Q

GDP role in overall healthcare of OSCC pt

A

1 - pre-tx phase: be involved, be present at tumour board, make accurate and appropriate recommendations
2 - post-tx phase: help in alleviating pain and discomfort due to tx
3 - long-term followup: advise pt in maintaining good OH and attending regular dental visits

309
Q

high risk HPV

310
Q

how long does high risk HPV infection typically last?

A

12-18 months before eventually being cleared by immune system

311
Q

when can dysplasia from HPV16 or 18 arise?

A

when the host immune system fails to clear and it persists for a long time

312
Q

describe the oncogenic HPV function pathway if the immune system fails to clear it

A

viral E2 protein (a negative regulator of E6+7) function gets abrogated
over expression of main viral oncoprotein E6+7
subsequent inhibition of the TSPs p53 and pRb (retinoblastoma protein) pathways
leads to inhibition of interferon response, activation of telomerase, promotion of cell divisions, immortalisation and transformation
causes genetic instability with unregulated cell replication and accumulation of aberrant chromosomal mutations, which cause dysplasia of varying degrees

313
Q

why can’t early diagnosis of HPV-related OSCC be accurately established?

A

because clinical lesions of early HPV-related lesions are unknown

314
Q

what does HPV+ OSCC have a significant association with?

A

history of suspicious Pap results of the cervix in females

315
Q

what risk do unvaccinated pts for HPV have of developing OPC?

316
Q

why is there a genetic susceptibility to cancer?

A

because carcinogenesis is a multistep process at both the phenotypic and genetic levels, resulting from the accumulation of multiple mutations

317
Q

acquired (env) DNA damaging agents

A

chemicals
radiation
viruses

318
Q

2 types of inherited mutations

A

genes affecting DNA repair

genes affecting cell growth or apoptosis

319
Q

why do you get mutations in genome of somatic cells?

A

failure of DNA repair and inherited mutations

320
Q

3 effects of mutations in genome of somatic cells

A

activation of growth-promoting oncogenes
inactivation of TSGs
alterations in genes that regulate apoptosis

leads to

unregulated cell proliferation and decreased apoptosis

which leads to clonal expansion

321
Q

from clonal expansion what contributes to tumour progression?

A

angiogenesis
escape from immunity
additional mutations

322
Q

what 3 factors combine to to ensure a proper env for malignant development?

A

genetic events
risk factors
epigenetic mechanisms

323
Q

what are epigenetic events?

A

“heritable phenotype changes that do not involve alterations in the DNA sequence”

324
Q

give 3 examples of epigenetic events

A

DNA methylation
histone modifications
miRNAs

Oral medicine (14 decks)

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