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head and neck and cns > CNS Oncology & RT > Flashcards

CNS Oncology & RT Flashcards

1
Q

how many brain tumours are primary

A

80%

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2
Q

how many brain tumours are mets

A

20%

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3
Q

what does survival depend on

A

guaranteed survival or guaranteed fatality

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4
Q

how many types of brain tumour are there

A

130

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5
Q

what is the most common type of brain tumour

A

GBM

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6
Q

where can brain tumours be found

A

extra-axially and intra-axially

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7
Q

what are brain tumours graded on

A

genetic findings
PS + fitness
extent of spread
tumour type
location
tumour left after surgery, the amount affects the grade and outcome

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8
Q

what is extra-axial

A

outside the brain
meningioma, acoustic neuroma

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9
Q

what is intra-axial

A

inside the brain
glioma

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10
Q

what information enhances treatment options

A

genetics

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11
Q

what genetics can be looked at

A

gaining or losing a chromosome, could swap position with other DNA
DNA mark up can change its behaviour

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12
Q

what is MGMT responsible for

A

cell repair
tumours have a high level, rapid cell repair therefore damage to cell via treatment is less effective

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13
Q

what is EGFR

A

Epidermal Growth Factor Receptor
protein involved in cell repair

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14
Q

what is IDK

A

isocitrate dehydrogenase
provides instructions for making a protein involved in cellular metabolism [energy production, cell repair can occur, harder to treat]

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15
Q

what is a seizure

A

an abnormal electroactivity burst within the brain

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16
Q

how are CNS tumours staged

A

using the 5th edition of WHO classification
no N stage [TNM IS NOT USED]
molecular grading: low grades can still be aggressive with some molecular subtypes

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17
Q

what are presenting symptoms

A

fatigue
confusion
sensitivity to light
pain
aching
eye movement issues
heavy body
early/late puberty
nausea & vomiting
balance issues
seizures
changes in head circumference
poor vision
headaches
throbbing head

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18
Q

what are some parietal presentations

A

visuo-spacial processing issues
knowledge of numbers
spelling
perception issues
object classification
processing info issues, close to the outside of the brain

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19
Q

how are they diagnosed

A

biopsy not always possible
imaging
MRI
CT [extra-axial]
PET-CT

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20
Q

how is a tumour properly diagnosed

A

imaging, lumbar puncture, angiography

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20
Q

why is a angiography useful

A

determines if the tumour has its own blood supply, identify any blockage
however it is unreliable for brain tumours

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21
Q

what is the job of the lumbar puncture

A

identify if there is any micromets present within the CSF fluid [determine spread]

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22
Q

what are the side effects/ management for CNS

A

short term memory loss
confusion
loss of fine motor skills
headaches = medication
dizziness
funny smell [irradiated olfactory nerve]
altered PS
vision changes
nausea and vomiting
balance and coordination
seizures = medicine
fatigue
hair loss

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23
Q

how are side effects managed

A

steroids
anti-convultants i.e keppra
SLT
antisickness
counselling
family support
physiotherapy
consent [Mental Health Capacity Act 2005]

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24
Q

what is the mental capacity act

A

understand info about decision
remember the info
consider in the decision making process
communicate their decision

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25
Q

what are gliomas

A

a group of tumours, which arise from glial cells the most common are astrocytes and oligodendrocytes

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26
Q

what are gliomas characterised on

A

the genetic mutation
DNA mark up is important

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27
Q

what are the types of gliomas

A

astrocytoma
ogliodendroglioma
gliobastoma

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28
Q

what is an astrocytoma

A

tumour from astrocyte cells, found in WM, the EGFR is high which promotes tumour growth

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29
Q

what is a grade 1 astrocytoma

A

pilocytic astrocytoma:
slow growing
cerebellum/optic pathway
well defined edges within capsule
good for surgical removal, low risk of recurrence
occur in <20

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30
Q

what is a grade 2 astro

A

diffuse astro
undefined edges
20-45
can cause a recurrence, a recurrent grade 2 = grade 3

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31
Q

what is a grade 3 astro

A

anaplastic:
rapid division
often recur to become grade 4 glioma
30-70
might need a debulking treatment

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32
Q

what is a ogliodendroglioma

A

occurs from the oligodendrocytes [conductor between neurons]
40-60
2-5% of primary CNS
G1= rare
G2 = slow growing
G3 =. rapid growth
mostly occur on the brain but can be found in the SC
frontal and temporal are the most common lobes
seizures, convulsions, slow motor responses, behavioural changes

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33
Q

what genetic difference does a gliobastoma have

A

EGFR amplification = 40%

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34
Q

HGG

A

high grade glioma

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35
Q

LGG

A

low grade glioma

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36
Q

what are the different types of glioblastoma HGG

A

IDH wildetype
multiforme
giant cell GB
gliosarcoma
epitheloid GB

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37
Q

how many primary CNS are glioblastomas

A

54%
have a <2 year prognosis

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38
Q

characteristics of a HGG glioblastoma

A

significant damage to neurological function
diffuse infiltration to other parts of the brain
frequently crosses midline, involving the contralateral brain
resistant to treatment
HGG grow with an expanding and destructive process

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39
Q

where are patterns for GB found

A

in the subcortical WM and deep GM of the central hemispheres particularly in the temporal lobe

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40
Q

what is the mandatory criteria for a GBM

A

16+
diffuse astrocytic
IDH wildetype

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41
Q

what is the criteria that a GBM must have one of

A

necrosis
microvascular proliferation
TERT promoter mutation
EGER gene amplification
gain 7 chromosome and loss 10 chromosome

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42
Q

where is a primary extra-axial tumour found

A

outside the cerebrum

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43
Q

what type of tumour is a menigioma

A

extra-axial

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44
Q

describe a meningioma

A

slow growing
in the arachnoid layer
25% of primary CNS
presentation occurs when its highly infiltrated intracranially

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45
Q

what is the options for a meningioma

A

active monitoring
RT for symptomatic patients
surgery
NO chemo as it doesnt respond

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46
Q

why are skull based tumours difficult to treat

A

sit close to the CNS and brainstem

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47
Q

what tumours arise from neuromuscular structures

A

meningioma
pituitary adenoma
schwannoma

48
Q

what tumours arise from the cranial base

A

chordoma
chondrosarcoma

49
Q

what is a schwannoma tumour presentation
[trigeminal nerve/ vestibular schwannoma]

A

unilateral hearing loss = 90%
severe pain
facial numbness
brain stem compression = 60-80%
very difficult to treat

50
Q

germinoma

A

kids + young adults
arise from germ cells
havent properly formed + migrated
spread via CSF

51
Q

craniopharyngioma

A

near pituitary
bengin
PBT
eye/ sight problems, headaches and tiredness

52
Q

ependymoma

A

arise from ependymal cells
SIOP II trial looks at chemo as an addition + RT extension

slow growing
surgery alone + RT
localised ependymoma = 42 days [28 is ideal]

53
Q

what is the trial RT regime for ependymoma

A

phase I: whole CNS
36Gy in 20 >3cm
25Gy in 20 < 3

phase II: tumour bed boost + boost to met sites
up to 59.4Gy in 33 [50.4 for spine mets]

54
Q

what is ependymoma presentation

A

neck pain, tingling in hands and neck swelling

55
Q

what is the RT for ependymoma

A

VMAT [however there is dose issues]
54Gy in 30

56
Q

what is the risks for spinal cord tumours

A

they are unknown apart from NF1/NF2 mutations

57
Q

NF1 mutations include.

A

high levels of skin pigmentation
multiple tumours along spine/ brain
growth disorder
intellectual impairment

58
Q

what is upper body presentation

A

arm weakness
respiratory
pain
pins in needles

59
Q

what is lower body presentation

A

leg weakness
problems walking
bladder/bowel control
sexual function
pain
pins in needles

60
Q

what are intramedullary tumours

A

within the nerves of the SC
astrocytomas and ependymomas

61
Q

what are intradural extramedullary tumours

A

start inside the SC coverings but outside the cord not within the nerve tissue
meningiomas and schwannomas

62
Q

what are extra-dural spine tumours

A

tumours which start within the spine bone, which is a primary

63
Q

what are some benign extradural spine tumours

A

oesteomas and oesteoblastomas

64
Q

what are some malignant extradural spine tumours

A

oestosarcomas, chondrosarcomas, fibrosarcomas

65
Q

what is a chordoma

A

a tumour which arises from the base of skull or spine
it is slow growing, so it uses a watch and wait approach
if fast then surgery will occur

66
Q

what is a chondrosarcoma

A

the most common primary bone tumour which arises from the cartilage cells
common in >40
which presents as a physical lump

67
Q

what is the diagnosis for a spinal tumour

A

biopsy [must be safe]
blood test
lumbar puncture
bone scan [any bone mets]

67
Q

where is spread likely for spine tumours

A

nearby tissues/ up or down the spine

68
Q

brain tumour -> spine

A

common

69
Q

spine tumour -> brain

A

uncommon

70
Q

do spine tumours require a high or low dose

A

high because they are radio-resistant
SHOULDNT BE HYPOFRACTIONATED

71
Q

what is the treatment for SC tumours

A

most common = watch and wait
debulking is only if there is a paralysis risk
if surgery cant happen RT will, also if unable to remove the entire tumour, after debulking surgery or after surgery to prevent recurrence

72
Q

what type of RT is ideal

A

PBT
if not then SABR then SRS

protons allow for dose escalation, beam shaping however the patient must have clear surgical margins, no micro spread and no metal work
useful at sparing healthy tissue and reducing secondary malignancies

73
Q

what is the PBT dose for spinal cord tumours

A

75.6Gy/CGE/ 42 fractions

74
Q

how many hours must be given between each treatment for SBAR

A

40

75
Q

what type of cancer is SABR for

A

oligo met

76
Q

what is the inclusion criteria for SBAR

A

spinal oligo met
PS 0-2
limited systemic disease
<2 consecutive vertebral bodies involved
3-5mm away from cord
well defined
18+
histological confirmation of neoplastic disease

77
Q

what is the exclusion criteria for SABR

A

spinal instability
unable to tolerate RT
pacemaker/metal work
prognosis< 3 months
significant or progressive neurological deficit
emergency surgery or RT
radiosensitive histology
SC compression

78
Q

what is the spine doses for SABR

A

1 fraction = 18-24Gy
2 fractions = 24Gy
3 alt days or daily = 24-27Gy

79
Q

what determines the treatment for CNS tumours

A

identify the tumour genetics
tumour location, size,
PS
what will be beneficial whilst reducing the impact of QOL
age
low or high risk
molecular/genetic status
LE > 12 weeks

biopsy helps identify any resistance

80
Q

what happens as PS decreases

A

the fractionation decreases

81
Q

what is the planning for CNS

A

CT
head in neutral = lateral
head tilt = frontal or occipital
supine + mask
protons can be done prone for posterior tumours

82
Q

what is the dose constraint for BS

A

<54

83
Q

dose constraint for retina

A

< 45

84
Q

dose constraint for optic chiasm

A

<45 due to risk of blindness however can be 50-54

85
Q

dose constraint for cochlea

A

< 50

86
Q

dose constraint for lens

A

< 10 Gy but ideally < 6

87
Q

are high or low doses needed for GBM

A

high as they are high grade made up of multiple cell types

88
Q

whats the dose for GBM IDH wildetype good PS

A

60Gy in 30 in 6 weeks +/- temz

89
Q

whats the dose for GBM IDH wildetype moderate PS

A

40Gy in 15 in 3 weeks +/- temz

90
Q

whats the dose for GBM IDH wildetype low PS

A

34Gy in 10 fractions or 30Gy in 6 on alternate days

91
Q

what treatment cant be used for craniopharyngioma

A

surgery

92
Q

what is the fractionation for craniopharyngioma

A

50.1-54Gy in 30

93
Q

what is the beam arrangement for craniopharyngioma

A

field borders
reids baseline
base of orbit EAM
sup/ant + post into air to cover whole brain
MLC = reduced dose to eye into air to reduce scatter

94
Q

what is the SRS potential dependent on for meningioma

A

size
small volume (5mm from optic apparatus)

hypofractionated SRS for smaller meningioma <3cm 25Gy in 5

95
Q

whole brain fractionation for grade 1

A

VMAT 50-54Gy in 25-30
SRS 13-15Gy in 1
SRS 25Gy in 5

96
Q

whole brain fractionation Grade 2

A

54-60Gy in 30

97
Q

whole brain fractionation Grade 3

A

60Gy in 30

98
Q

what is the time period for cord comp

A

24 hours
fast tracked if hand numbness
48 hours if it is an accidental finding and asymptomatic

99
Q

what scan is done to look at the areas need to be treated for CC

A

MRI/CT
whole spine

100
Q

CC dose for < 6 months

A

8Gy in 1

101
Q

CC dose for good prognosis/ post spine surgery

A

20Gy in 5
30Gy in 10

102
Q

what is the RT technique for CC

A

simple open fields
single applied field
extended FSD
6/10MV (L = 10MV)
1 vertebrae above and 1 below
CT scanned, field applied on prosoma

103
Q

what are the SE and management to CC RT

A

antisickness (field size + location)
worsening of neurological symptoms
worse tingling
increased pain
skin reaction = treating at D-max
diarrhoea
oesophagitis

104
Q

what is a late effect of CC RT

A

radiation neuropathy
destruction of the myelin sheath, worse sensory issues

105
Q

steroid SE

A

insomnia
low mood
mood swings
weight gain - water retention
increased appetite

prolonged use
loss of muscle mass
immunosuppression
cataracts
bone density changes
personality changes

106
Q

what deletions have the worse prognosis

A

1p/19q

107
Q

what is the dose for G2 of 1p/19q deletion

A

50.4Gy in 28
45Gy in 25 or 54 in 30 with adj PCV or temz

108
Q

what is the dose for G3 of 1p/19q deletion

A

59.4Gy in 33 with adj temz

109
Q

what is the dose for G4 of 1p/19q deletion

A

60Gy in 30 +/- concurrent + adj temz

110
Q

what are the brain met treatment options

A

gamma knife = solitary + mets = total volume 20cm cubed
cyber knife
PBT
WBRT +/- hippocampal sparing

111
Q

what are the doses for WBRT

A

20Gy in 5 (pall)
30Gy in 10 6MV

whole brain RT reduces QOL however disease control

112
Q

what is the dose for 1 fraction SRS for <20mm

A

21-24

113
Q

what is the dose for 1 fraction SRS for 21-30mm

A

18

114
Q

what is the dose for 1 fraction SRS for 31-40mm

A

15 can also consider hypo

115
Q

what is the dose for hypofraction SRS

A

24-27Gy in 3 daily
30Gy in 5 daily
35Gy in 5 daily

116
Q

why should gamma knife not be done for volumes greater than 20

A

greater risks

head and neck and cns (12 decks)

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