CNS Oncology & RT Flashcards

(118 cards)

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
what is the mental capacity act
understand info about decision remember the info consider in the decision making process communicate their decision
25
what are gliomas
a group of tumours, which arise from glial cells the most common are astrocytes and oligodendrocytes
26
what are gliomas characterised on
the genetic mutation DNA mark up is important
27
what are the types of gliomas
astrocytoma ogliodendroglioma gliobastoma
28
what is an astrocytoma
tumour from astrocyte cells, found in WM, the EGFR is high which promotes tumour growth
29
what is a grade 1 astrocytoma
pilocytic astrocytoma: slow growing cerebellum/optic pathway well defined edges within capsule good for surgical removal, low risk of recurrence occur in <20
30
what is a grade 2 astro
diffuse astro undefined edges 20-45 can cause a recurrence, a recurrent grade 2 = grade 3
31
what is a grade 3 astro
anaplastic: rapid division often recur to become grade 4 glioma 30-70 might need a debulking treatment
32
what is a ogliodendroglioma
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
33
what genetic difference does a gliobastoma have
EGFR amplification = 40%
34
HGG
high grade glioma
35
LGG
low grade glioma
36
what are the different types of glioblastoma HGG
IDH wildetype multiforme giant cell GB gliosarcoma epitheloid GB
37
how many primary CNS are glioblastomas
54% have a <2 year prognosis
38
characteristics of a HGG glioblastoma
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
39
where are patterns for GB found
in the subcortical WM and deep GM of the central hemispheres particularly in the temporal lobe
40
what is the mandatory criteria for a GBM
16+ diffuse astrocytic IDH wildetype
41
what is the criteria that a GBM must have one of
necrosis microvascular proliferation TERT promoter mutation EGER gene amplification gain 7 chromosome and loss 10 chromosome
42
where is a primary extra-axial tumour found
outside the cerebrum
43
what type of tumour is a menigioma
extra-axial
44
describe a meningioma
slow growing in the arachnoid layer 25% of primary CNS presentation occurs when its highly infiltrated intracranially
45
what is the options for a meningioma
active monitoring RT for symptomatic patients surgery NO chemo as it doesnt respond
46
why are skull based tumours difficult to treat
sit close to the CNS and brainstem
47
what tumours arise from neuromuscular structures
meningioma pituitary adenoma schwannoma
48
what tumours arise from the cranial base
chordoma chondrosarcoma
49
what is a schwannoma tumour presentation [trigeminal nerve/ vestibular schwannoma]
unilateral hearing loss = 90% severe pain facial numbness brain stem compression = 60-80% very difficult to treat
50
germinoma
kids + young adults arise from germ cells havent properly formed + migrated spread via CSF
51
craniopharyngioma
near pituitary bengin PBT eye/ sight problems, headaches and tiredness
52
ependymoma
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
what is the trial RT regime for ependymoma
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
what is ependymoma presentation
neck pain, tingling in hands and neck swelling
55
what is the RT for ependymoma
VMAT [however there is dose issues] 54Gy in 30
56
what is the risks for spinal cord tumours
they are unknown apart from NF1/NF2 mutations
57
NF1 mutations include.
high levels of skin pigmentation multiple tumours along spine/ brain growth disorder intellectual impairment
58
what is upper body presentation
arm weakness respiratory pain pins in needles
59
what is lower body presentation
leg weakness problems walking bladder/bowel control sexual function pain pins in needles
60
what are intramedullary tumours
within the nerves of the SC astrocytomas and ependymomas
61
what are intradural extramedullary tumours
start inside the SC coverings but outside the cord not within the nerve tissue meningiomas and schwannomas
62
what are extra-dural spine tumours
tumours which start within the spine bone, which is a primary
63
what are some benign extradural spine tumours
oesteomas and oesteoblastomas
64
what are some malignant extradural spine tumours
oestosarcomas, chondrosarcomas, fibrosarcomas
65
what is a chordoma
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
what is a chondrosarcoma
the most common primary bone tumour which arises from the cartilage cells common in >40 which presents as a physical lump
67
what is the diagnosis for a spinal tumour
biopsy [must be safe] blood test lumbar puncture bone scan [any bone mets]
67
where is spread likely for spine tumours
nearby tissues/ up or down the spine
68
brain tumour -> spine
common
69
spine tumour -> brain
uncommon
70
do spine tumours require a high or low dose
high because they are radio-resistant SHOULDNT BE HYPOFRACTIONATED
71
what is the treatment for SC tumours
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
what type of RT is ideal
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
what is the PBT dose for spinal cord tumours
75.6Gy/CGE/ 42 fractions
74
how many hours must be given between each treatment for SBAR
40
75
what type of cancer is SABR for
oligo met
76
what is the inclusion criteria for SBAR
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
what is the exclusion criteria for SABR
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
what is the spine doses for SABR
1 fraction = 18-24Gy 2 fractions = 24Gy 3 alt days or daily = 24-27Gy
79
what determines the treatment for CNS tumours
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
what happens as PS decreases
the fractionation decreases
81
what is the planning for CNS
CT head in neutral = lateral head tilt = frontal or occipital supine + mask protons can be done prone for posterior tumours
82
what is the dose constraint for BS
<54
83
dose constraint for retina
< 45
84
dose constraint for optic chiasm
<45 due to risk of blindness however can be 50-54
85
dose constraint for cochlea
< 50
86
dose constraint for lens
< 10 Gy but ideally < 6
87
are high or low doses needed for GBM
high as they are high grade made up of multiple cell types
88
whats the dose for GBM IDH wildetype good PS
60Gy in 30 in 6 weeks +/- temz
89
whats the dose for GBM IDH wildetype moderate PS
40Gy in 15 in 3 weeks +/- temz
90
whats the dose for GBM IDH wildetype low PS
34Gy in 10 fractions or 30Gy in 6 on alternate days
91
what treatment cant be used for craniopharyngioma
surgery
92
what is the fractionation for craniopharyngioma
50.1-54Gy in 30
93
what is the beam arrangement for craniopharyngioma
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
what is the SRS potential dependent on for meningioma
size small volume (5mm from optic apparatus) hypofractionated SRS for smaller meningioma <3cm 25Gy in 5
95
whole brain fractionation for grade 1
VMAT 50-54Gy in 25-30 SRS 13-15Gy in 1 SRS 25Gy in 5
96
whole brain fractionation Grade 2
54-60Gy in 30
97
whole brain fractionation Grade 3
60Gy in 30
98
what is the time period for cord comp
24 hours fast tracked if hand numbness 48 hours if it is an accidental finding and asymptomatic
99
what scan is done to look at the areas need to be treated for CC
MRI/CT whole spine
100
CC dose for < 6 months
8Gy in 1
101
CC dose for good prognosis/ post spine surgery
20Gy in 5 30Gy in 10
102
what is the RT technique for CC
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
what are the SE and management to CC RT
antisickness (field size + location) worsening of neurological symptoms worse tingling increased pain skin reaction = treating at D-max diarrhoea oesophagitis
104
what is a late effect of CC RT
radiation neuropathy destruction of the myelin sheath, worse sensory issues
105
steroid SE
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
what deletions have the worse prognosis
1p/19q
107
what is the dose for G2 of 1p/19q deletion
50.4Gy in 28 45Gy in 25 or 54 in 30 with adj PCV or temz
108
what is the dose for G3 of 1p/19q deletion
59.4Gy in 33 with adj temz
109
what is the dose for G4 of 1p/19q deletion
60Gy in 30 +/- concurrent + adj temz
110
what are the brain met treatment options
gamma knife = solitary + mets = total volume 20cm cubed cyber knife PBT WBRT +/- hippocampal sparing
111
what are the doses for WBRT
20Gy in 5 (pall) 30Gy in 10 6MV whole brain RT reduces QOL however disease control
112
what is the dose for 1 fraction SRS for <20mm
21-24
113
what is the dose for 1 fraction SRS for 21-30mm
18
114
what is the dose for 1 fraction SRS for 31-40mm
15 can also consider hypo
115
what is the dose for hypofraction SRS
24-27Gy in 3 daily 30Gy in 5 daily 35Gy in 5 daily
116
why should gamma knife not be done for volumes greater than 20
greater risks