brain tumours Flashcards
most common brain tumour
metastatic carcinoma
what are the 2 things you need to figure out when you’re discussing brain tumour
intra-axial vs extra-axial
primary vs secondary
describe types of glial cells and their tumours
atrocytes = maintain BBB
oligodendrocytes = meylin
ependymal cells = line ventricular system + central spinal canal
artocytomas, oligodendrogliomas, ependymomas
presentation of brain tumour symptoms
headaches = inc ICP
focal neurological deficit
seizures
describe astocytomas
80% adult primary brain tumours
CNS
4th - 6th decade
macroscopic appearance of atrocytomas
diffuse = poorly edfined infiltrative tumour, expands, distorts surrounding brain
glioblastoma = variability in appearance throughout tumour, heam, necrosis (contrast enhancement), appear deceptively well-demarcated
how do we grade astrocytoma
amen
atypia, mitoses, endothelial proliferation, necrosis
atypia alone = grade 2
with mitoses = grade 3
with necrosis/ endothelial proliferation = grade 4
describe the histology of astrocytomas
moderate inc cellularity + variable degrees nuclear pleommorphism
anaplastic astrocytoma = additional features mitotic activity
glioblastoma = additional features nectorsis/vascular proliferation
describe pseudopalisading necrosis
hypoxia -> migration -> necrosis + palisade -> angiogenesis + clonal selection
describe diffuse astrocytoma
WHO grade 2
10-15% astrocytic brain tumours
peak incidence young adults 30-40
imaging = lack enhancement
differential diagnosis = distinction from reactive astrocytes
what is gemistrocytic astrocytomyrs
20% tumour cells in diffuse astrocytoma
prone to progression to anaplasitc astrocytoma/GBM
considered WHO grade 2
surivial time = 6-8
length disease affected byr/prog to GBM = avg 4.5 urs
no predictor of when/whether prog is likely
anaplastic astrocytoma
WHO grade 3
sample size in assessing mitotic activity, /multinucleated cells, abnormal mitoses
intermediate stage on way to GBM
strong tendency to progress within 2 yers
glioblastoma
WHO grade 4
most frequent
45-75 yrs
cycstic necrosis, c/f cysts in low grade lesions
rapid growth + infiltration, necrosis/endo proliferation
rarely invades SAS/CSF
heam spread rare wo/surgery or invasion dura/bone
primary glioblastoma
rapidly progressive, without pre-existing low grade tumour
older patients
amp EGFR gene, MDM2 overexpression, p16 deletion, PTEN mutation
secondary glioblastoma
young patients w/previously diagnosed low grade astrocytic tumour
glioblastoma invasion
invasive phemotype = early on invasion of white matter
- perineuronal satellitosis, perivasular growth, subpail spread
combo of migration + modulation of EC space
hard to cut out
distinct from invasion of carinomas into adj tissues
how do glioblastomas affect ECM
distinct from invasion of carcinmas bc change nature ECM = mainly hyaluronic aci, except around bv & pial surface
cel-cell and cell-EC amtrix interactions
proteases degrade EC + remodel env to facilitate tumour growth
integrin rec interact w/mol in ECM -> locomotion
describe oligodendrogliomas
5-15% gliomas
4th -> 5th decade
long history symptoms, seizures
cerebral hemispheres esp white matter
morphology ofoligodendrogliomas
circumscribed, gelatinous massess
calcification common radiology
sheets fried egg cells w/ characteristic vascular pattern + calcification
low rate mitotic act
anaplastic + hybrid variants
describe genetic of oligodendrogliomas
loss heterozygosity )LOH) of 1p + 19q
prognositc importance and response to chemo
describe ependymomas
arise near ventricles + spinal canal
chilren = 4th ventricle
adults= spinal canal
describe ependymomas morphology
solid papilllary mass arising from floor of centricle
round to oval nuclei, dense fibrillar background + rosette + perivascular pseudorosette formation
well differentiated + behaves as WHO grade II
clinical features of ependymomas
posterior fossa ependymomas = hydrocephalus bc obstruction 4th ventricle
CS dissemination = common
avd survival 4 yrs
