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Medicine Phase 2a Neuro > Primary and secondary brain tumours > Flashcards

Primary and secondary brain tumours Flashcards

1
Q

Incidence of all brain tumours

A

~20:100,000
16th most common registered adult cancer
2nd most common paediatric cancer

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2
Q

Incidence of primary tumour

A

~8:100,000

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3
Q

Presentation of a brain tumour - 3 cardinal presenting symptoms

A

Symptoms of raised ICP (headache, reduced conscious level, nausea and vomiting)
Progressive neurological deficit
Epilepsy

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4
Q

Causes of raised ICP (intracranial pressure)

A

Headache
Drowsiness
Vomiting

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5
Q

Features of raised ICP headache

A

Worst on waking from sleep in morning
Increased by coughing, straining and bending forwards
Sometimes relieved by vomiting

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6
Q

Cardinal physical sign of raised ICP and its cause

A 
Papilloedema
Due to obstruction of venous return from the retina
Loss of crisp optic nerve head margins
Venous engorgement
Retinal oedema
Haemorrhages
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7
Q

What is papilloedema

A

optic disc swelling that is caused by increased intracranial pressure

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8
Q

Focal neurological deficits

A 
Motor deficit (this includes ataxia)
Sensory deficit
Speech deficit
Visual deficit
Deafness
Deteriorating memory
Personality change
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9
Q

Features of epilepsy as a result of brain tumour

A

Sinister when of recent onset
Focal seizures more common with tumours:
Motor, Sensory, Temporal lobe pattern
(olfactory aura or ‘deja vue’)

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10
Q

Types of brain tumours

A

Primary

Secondary

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11
Q

Are primary or secondary tumours more common

A

Secondary

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12
Q

Aetiology of secondary tumours

A

Non small cell LUNG 24%
Small cell LUNG 15%

Breast 17%
Melanoma 11%
Renal cell 6%
GI 6%
Unknown primary 5%
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13
Q

Secondary brain tumour treatment options

A

Surgery
Radiotherapy
Chemotherapy
Best supportive care

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14
Q

When is surgery considered as an option for brain cancer patients

A

Absent or controlled 1st degree disease i.e. survival >1/4
Age <75
Good performance status

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15
Q

Median survival from surgery

A

13.4 months
(1 yr survival 56%)
(5yr survival 15%)

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16
Q

Surgical failure rate for brain tumour

A

52% of radiation group had brain recurrence

28% of surgery and radiation group had recurrence

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17
Q

What cell type are majority of primary brain tumours from

A

Glial cells

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18
Q

Types of primary brain tumours

A

Astrocytoma (85-90%)
Oligodendroglioma (~5%)
Others: medulloblastoma, central neurocytoma etc

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19
Q

WHO Grading of Gliomas

A

Grade I - Paediatric tumour/pilocytic astrocytoma
Grade II - Premalignant tumour (benign)
Grade III - Anaplastic astrocytoma (cancer)
Grade IV - Glioblastoma multiforme (GBM) - Most common phenotypes

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20
Q

True or False:

Given enough time all gliomas will progress inexorably to become GBM (glioblastoma multiforme)

A

True

21
Q

Pathophysiology to malignant glioma

A

2 ways:
1. (More Common) Initial genetic error is of glucose glycolysis:
Mutation of isocitrate dehydrogenase 1 (IDH-1). Results in excessive build up of 2-Hydroxyglutarate. Which triggers genetic instability in glial cells and subsequent inappropriate mitosis.
2. No IDH mutation:
Catastrophic genetic mutation. Very poor prognosis even for ‘low grade’ tumours.

22
Q

Survival of glioblastoma

A

At present under 20% survive of patients with GBM survive more than 18 months from diagnosis even with ‘aggressive therapy’

23
Q

Good prognostic factors of glioblastoma patient

A

Age under 45-50 years
Aggressive surgical therapy
Good performance post surgery
Tumour that has transformed from a previous low grade tumour (secondary GBM)
MGMT mutant – which means they should respond chemoRx

24
Q

Poor prognostic factors of glioblastoma patient

A

> 50 years
Post-surgery: Poor neurological function - drowsy, headache, focal neurology
Non radical surgical treatment
De novo disease: Primary GBM
MGMT ‘wild type’ - no predicted response chemoRx

25
Q

Glioblastoma therapy

A

Resective surgery if possible
Adjuvant chemotherapy with TEMOZOLOMIDE at time of RT (60Gy)
Followed up by Temozolomide chemoRx
6 cycles (5/7 every 4/52 for 6/12 or to progression).

26
Q

How does Temozolomide work?

A

Prodrug activated by HCl
Crosses BBB
Methylates guanine in DNA making replication impossible at this base site

27
Q

How can you reverse Temozolomide

A

MGMT (Methyl-Guanine-Methyl-Transferase)
MGMT reverses guanine methylation by Temozolomide

Example of tumour resistance to Temozolomide (enzyme that can be made by cancerous cells)

28
Q

Unproven treatment of glioblastoma

A

Anti angiogenic Rx (Bevazicumab ‘AVASTIN’) - tho doesnt benefit survival time
Anti angiogenic agent that shuts down tumour blood supply

29
Q

When would you use ‘suicide gene therapy’ and how does it work

A 
Involves inocculation of tumour with replication deficient HSV-1 retrovirus.
Wild type HSV-1 replicates exponentially and causes encephalitis.
Replication deficient (modified) HSV-1 fails to replicate in normal brain – i.e. non virulent.
Modified HSV-1 replicates with the rapidly dividing cells (GBM) -  subsequent oncolysis results in release of progeny virus – selective replication competence
Tumour cells killed normal brain cells unaffected.
30
Q

What is dexamethasone

A

Most powerful synthetic steroid
Rapidly improves brain performance in all brain tumours
Reduces tumour inflammation/oedema

31
Q

Palliative care for glioblastoma

A

MacMillan nurses
Hospice
Complementary therapy

32
Q

What grade is a benign glioma

A

Low grade glioma II

33
Q

Epidemiology of benign glioma

A

Disease of young adults (rare >45 years old)

Commonly presents with seizures as first symptom

34
Q

Median survival from diagnosis of benign glioma

A

5-7 years

35
Q

Cause of deterioration from benign glioma

A

Tumour transformation to a malignant phenotype.
Progressive mass effect due to slow tumour growth.
Progressive neurological deficit from functional brain destruction by tumour.

36
Q

Survival from oligodendroglioma

A

10-15 years survival

37
Q

Features of oligodendroglioma

A

Will transform to anaplastic (WHO 3) variant eventually
Can transform to GBM
Genetic defect in chromosome 1 and 19

38
Q

Treatment of oligodendroglioma

A

(triple agent) chemotherapy

39
Q

WHO Grading of Gliomas

A

Grade I - Paediatric tumour/pilocytic astrocytoma
Grade II - Premalignant tumour (benign)
Grade III - Anaplastic astrocytoma (cancer)
Grade IV - Glioblastoma multiforme (GBM) - Most common phenotypes

40
Q

Prognosis of each grade of glioma

A

I - good
II - >5 years
III - 2-5 years
IV - <1 year

41
Q

Describe grade I glioma

A

Completely benign

Paediatric tumour - mainly see in children

42
Q

Describe grade II glioma

A

Premalignant tumour

43
Q

Describe grade III glioma

A

CANCER! - Malignant

See active growth & mitotic activity on microscope

44
Q

Describe grade IV glioma

A

MOST COMMON PHENOTYPE
Active growth, mitotic activity, necrosis (since growing so fast, it falls apart) and vascular
proliferation
VERY MALIGNANT

45
Q

Types of treatment of brain tumour

A

Surgical
Medical
Radiotherapy

46
Q

Treatment of brain tumour (surgical, medical and when to use radiotherapy)

A

Surgery: Exploration, removal or biopsy (meningiomas can be fully removed without incident)
Radiotherapy: Gliomas and radiosensitive metastases
Medical: Cerebral oedema can be reduced with corticosteroids. Epilepsy treated with anticonvulsants.

47
Q

Medical treatment of cerebral oedema

A

Corticosteroids

48
Q

Medical treatment of epilepsy

A

Anticonvulsants

49
Q

Diagnosis of brain tumour

A

CT and MRI

Positron Emission Tomography to find occult metastasis

Medicine Phase 2a Neuro (28 decks)

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