Brain tumours Flashcards

1
Q

Symptoms of a brain tumour

A

Focal (related to area of lesion) vs generalised
Non-localising e.g apathy, personality change, dementia, drowsiness
Localising
Lobar (FPTO)
Cranial nerve palsy, I,II, (III,IV,VI),V VII,VIII, (IX,X,XI) XII
Seizures- focal, generalised
Recognition of seizure vs TIA/ VV etc
Recognition of new onset- subtle neuro symptoms vs stress etc

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2
Q

Raised intracranial pressure

A

2/3rds patients with space occupying lesions have classical triad of
1. Headache
2. Papilledema
3. Vomiting (most remainder have at least 2 of these)
Many mental disturbances- drowsiness, coma, mild personality change or even profound dementia

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3
Q

Raised ICP- headache

A
On waking ( due to raised ICP after hours of lying supine)- can disappear for days or even weeks
Not greatly intense, throbbing or bursting- aggravated by coughing, sneezing, stooping down or exertion
Relieved by aspirin (bleeding) , codeine or going to bed?
Site may not give guide to tumour location- occ. headache radiating down neck can indicate post. fossa/ CP angle tumour
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4
Q

Raised ICP- vomiting

A

Before breakfast frequently as accompaniment of headache
Projectile- more occurs without nausea and without warning
Children more likely to vomit than adults- post. fossa tumour more likely to vomit than supratentorial tumours

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5
Q

Raised ICP- Visual symptoms (papillodema)

A

Often asymptomatic- vision eventually affected and number of tumours first detected by opticians
Enlargement of blind spot, late peripheral constriction of fields
Intermittent loss more common than steady deterioration- sitting up and lying down e.g morning
Sleeping may precipitate episodes of loss of vision

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6
Q

Types of IC tumour

A

Primary- arise within brain/ IC constituents e.g glioma( glial cells), meningiomas (arachnoid cap cellls), pituitary adenoma (pituitary cells), schwannomas (IC nerves)
Secondary- metastates from cancer elsewhere in body- typically lung and breast, but melanoma, renal cell, sarcoma and thyroid increased propensity to MS in brain

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7
Q

Gliomas

A
30% all brain tumours, 80% of all malignant 
Originate from 
Astrocytomas- astrocytes
Oligodendrogliomas- oligodendrocytes
Ependymomas- ependymal cells
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8
Q

Diffusely infiltrating astrocytomas

A

Develop to form mass but also diffusely infiltrate normal brain precluding complete surgical excision
II- low grade- slow growing, likely to eventually progress to malignant ( 5-7 yrs survival)
III- anaplastic astrocytoma- higher proliferation rate, more mitotically active (mean survival 2-3 years)
IV- glioblastoma- characterised histologically by elevated tumour cell proliferation, endothelial prolif, necrosis- mean survival 12-18 m

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9
Q

Treatment of gliomas- surgery

A

Obtain “tissue” (histological) diagnosis- closed biopsy, open via craniotomy
More definitve procedure when possible is tumour debulking of focal tumours to relieve mass/ pressure effect

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10
Q

Surgery- complications

A

May render patient disabled and unfit for subsequent oncological treatment
death, stroke like risks (speech, sensorimotor deficits, dyspraxia, hemianopia), haemhorrage, wound infection, seizures (eventually happen in majority of glioma patients)

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11
Q

Surgical techniques

A

Image guidance (detailed preop scans)
Real time- intra-operative imaging, e.g ultrasound, CT/MRI
Tumour fluorescence ie gliolan helps visualise malignant gliomas
Awake surgery with direct electrical stimulation and speech/physiotherapist monitoring

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12
Q

Radiotherapy- adjuvant for malignant gliomas

A

fractionated RT over 2-6 weeks
in assc. with temozolomide for glioblastomas- extended survival if methylation of MGMT promoter site (downregulate DNA damage repair gene, higher likelihood of tumour cell death)
Radiotherapy + PCV (procarbazine, lomustine, vincristine) chemotherapy for anaplastic oligodendrogliomas (deletion of 1p and 19q) may extend survival

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13
Q

Low grade gliomas

A

15% of new adult brain tumours, more likely in young adults- typically present with seizures, >90% resection delays time to malignant transformation and significantly extends overall survival

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14
Q

Meningiomas

A

Arachnoid cap cells of meninges- I (benign), II (atypical), III (malignant)
Majority benign and if resectable patient may be disease free- risk of local reccurence (follow ups)
Any small vol post surgery can be treated with highly precise radiation therapy
Tumours in deep seated locations, adherent to important BV’s, nerves (brainstem) may not be completely resectable mandating adjuvant SRS/ other radiotherapy
II- higher propensity to recur locally
III- frankly malignant

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15
Q

Brain metastases

A

primary sites lung, breast, melanoma, renal, thyroid- treatment depends on extent of primary/extracranial disease, expected prognosis, age and number/vol brain mets
surgical resection for solitary large tumours (pressure effects)
Stereotactic RadioSurgery
Whole brain radiotherapy (palliative)
Chemotherapy/ systemic anti-cancer treatment (biologics)

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16
Q

Childhood brain tumours

A

Pilocytic astrocytoma- complete resection may lead to normal life expectancy
Medulloblastoma- metastasise through CSF pathways including spine, patients usually require post-surgical radiotherapy ( CNS axis)- may require chemo
Ependymoma- not as aggressive as MB but tendency to recur/metastasise
Radiotherapy avoided under age 4 if possible-CNS toxicity on developing brain/CNS

17
Q

Cranial nerve tumours- schwannomas

A

slow growing benign nerve sheath tumours arising on vestibular nerve
-hearing loss, tinnitus, balance problems
associated with neurofibromatosis

18
Q

Pituitary adenoma

A

Large tumours- macroadenomas
compression of adjacent structures e.g optic nerves resulting in classical bitemporal hemianopia presentation

Small tumours- microadenomas
Prolactinoma
GH secreting (acromegaly)
ACTH- Cushing’s disease

19
Q

Palliative care

A

medication for management of symptoms
dexamethasone- peritumoral odeam
anti-seizure medication in tumour related epilepsy
Anti-emetics, analgesics- PCT, hospice

20
Q

How do tumours develop?

A

deregulated cell division, loss of normal checkpoint controls
stem cell hypothesis
angiogenesis- recruitment of blood supply to “feed” tumour
invasion/infiltration (gliomas) of surrounding brain tissue
Metastases develop from elsewhere and spread via bloodstream
Tumours can adapt- methylome/ methylation status