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X Clin Med III Exam 3 > CNS tumors > Flashcards

CNS tumors Flashcards

1
Q

Most common primary benign brain tumor

A

Meningioma

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2
Q

What do glial cells do?

A

Surround neurons and provide support, insulation and nutrients
Most abundant cell type in CNS

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3
Q

Types of CNS glial cells

A

Astrocytes
Ependymal cells
Oligodendrocytes
Microglia

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4
Q

Where does an astrocytoma originate?

A

Astrocyte (main glial supporting cell in CNS)”

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5
Q

Types of astrocytomas

A

Diffuse (cannot be resected completely and grade by WHO into grade I-IV based on histology)
Circumscribed

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6
Q

How to classify diffusely infiltrating gliomas of astrocytic and oligodendroglial lineage

A

Based on 2 recurrent and favorable molecular prognostic factors:
IDH mutation
1p/19q codeletion

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7
Q

WHO classification of most astrocytomas

A

IDH mutant

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8
Q

WHO classification of most oligodendogliomas

A

Both IDH mutant AND 1p/19q codeletion

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9
Q

Subclassifications of glioblastomas

A

IDH wildtype (most and worst prognosis)
IDH mutated
Glioblastoma not otherwise specified (NOS)

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10
Q

Malignant astrocytic neoplasms (HIGH GRADE GLIOMAS) are divided into 2 main groups

A

(based on degree of hypercellularity, nuclear pleomorphism, mitoses, microvascular proliferation and necrosis)

  • Anaplastic astrocytoma (AA, grade 3)
  • Glioblastoma multiforme (GBM, grade 4)
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11
Q

Presentation of anaplastic astrocytoma and glioblatoma multiforme

A

Short history of HAs, seizures, focal neuro sxs based on location
Predilection of extend across corpus callous of to spread along other major white matter tracts (butterfly)

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12
Q

How do malignant gliomas look on MRI?

A

Irregular mass lesions, heterogeneous or ring enhancing

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13
Q

MRI presentation of anaplastic astrocytoma and glioblatoma multiforme

A

T2W/FLAIR: abnormal signal extending in irregular pattern with extension beyond margins of contrast enhancement (usually infiltrating tumor cells in that area)

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14
Q

Most common and deadly glioma in adults

A

Glioblastoma multiforme

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15
Q

How to confirm glioblastoma multiforme

A

Imaging can suggest it but must do pathologic confirmation by biopsy or surgical resection
If can’t do that (b/c brainstem glioma), then do MR spectroscopy

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16
Q

Standard therapy for high grade glioma

A

1- maximal tumor resection with preservation of neuro function
2- limited field radiation therapy with 2-3 cm margin around radiographically visible tumor area (maybe chemo too)

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17
Q

Techniques for aggressive resection

A

Awake craniotomy
Diffusion tensor imaging or stimulation mapping to ID subcortical motor pathways
Intraoperative MRI

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18
Q

Prognosis of high grade gliomas

A

Most recur despite aggressive tx (6-8 month tumor progression)

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19
Q

Chemotherapy is best suited for which type of anaplastic oligodendroglioma

A

Codeleted 1p/19q

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20
Q

Types of supportive care for high grade gliomas

A 
Dexamethasome to reduce peri-tumor edema and increase neuro function
Pain and depression tx
Seizure therapy (non enzyme inducing antiepileptics)
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21
Q

Greatest prognostic factors in high grade gliomas

A

Pt age (>65 YO is worst)
Tumor histology
Pretreatment performance status
(median survival tho is 12-15 months)

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22
Q

How are low grade gliomas different from high grade?

A

Low tends to infiltrate rather than compress or destroy brain parencyma

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23
Q

How do most pts with low grade glioma present?

A

Seizures (can be partial)

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24
Q

Classification of most low grade gliomas

A

IDH mutations

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25
Q

Imaging of low grade gliomas

A

Poorly circumscribed lesions with diffuse infiltration

Hard to define gross and microscopic margins

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26
Q

What might help the diagnostic accuracy with low grade gliomas?

A

Tumor debulking

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27
Q

Which is more sensitive to chemo: oligodendrogliomas or astrocytomas

A

Oligodendrogliomas (has better prognosis too)

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28
Q

Where does oligodendroglioma originate?

A

Oligodendrocytes (produce myelin sheaths in CNS)

-low and high grade types

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29
Q

Classic histological features of oligodendrogliomas

A

Uniform round nuclei and clear perinuclear halos (fried egg) with network of branching capillaries (chicken wire)

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30
Q

Classification of most oligodendrogliomas

A

Most have 1p/19q co deletion (may also have TP53 mutation)

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31
Q

MRI for low grade astrocytoma

A

Poorly demarcated hypointense mass lesion on T1W images and hyperintense lesion on T2/FLAIR
GAD enhancement
Infiltration of tumor cells extends beyond margins or radiographically definable or grossly visible tumor

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32
Q

How does low grade oligodendroglioma look on MRI?

A

Ill defined non-enhancing lesion
High grade is heterogenous and ring enhacing
Tumor calcifications commonly seen
(cannot differentiate from astrocytic tumors solely with neuro imaging)

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33
Q

Younger pt with oligodendrogliomas and no neuro sxs

A

Defer surgery/RT (not negative impact if do so)

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34
Q

Why to prolong radiation as long as possible?

A

Can cause neurotoxicity

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35
Q

When to give radiation to pt with oligodendrogliomas?

A

Not candidate for aggressive tumor resecti on
Have large post op tumor burden
>50 YO at diagnosis

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36
Q

Indications of early intervention with oligodendroglioma and astrocytoma

A

Neuro sxs other than seizures
Presence of significant mass effect on imaging
Growth of lesion on serial scans
Age >50

37
Q

Prognosis of astrocytoma

A

Survival supratentorial astrocytoma 5-9 ys
Age at onset is strong independent predictor of survival outcome
Negative impact if significant neuro deficit or >50 at diagnosis
Favorable prognosis with long history of seizures and no other deficits

38
Q

What is present in most newly diagnosed low grade oligodendrogliomas

A

1p/q19 co deletion

39
Q

Importance of 1p/q19 co deletion with oligodendroglioma

A

Independent prognostic marker for less aggressive behavior, better response to tx (chemo) and better overall survival

40
Q

Where does meningioma come from?

A

Arachnoid cells

41
Q

Presence of meningioma

A 
Most asymptomatic (found on imaging or autopsy)
Symptomatic twice as comon in women (estrogen and progesterone receptors on tumor)
42
Q

Imaging for meningioma

A

Encircle on another, forming calcified whorls called psammoma bodies (solitary contrast enhancing lesions adjacent to dural surfaces)

43
Q

Classification of meningiomas

A

Grade 1: most and best to have
Grade 2: atypical and diagnosis made on brain invasion
Grade 3: malignant/anaplastic

44
Q

Common sites of origin for meningiomas

A

Cerebral convexity, parasagittal area, falx and sphenoid ridge

45
Q

Presentation of meningioma

A

Slow growth with slow progression of sxs
Hyperostosis in skull adjacent to tumor and this bone usually invaded by tumor cells
Peritumor edema

46
Q

Imaging for meningioma

A

MRA/MRV to determine blood supply in consideration for surgery or preop embolization

47
Q

Can you use chemo for meningiomas?

A

Not sensitive

48
Q

Therapy for meningioma

A

Defer tx until sxs develop or tumor enlarges

Symptomatic: total surgical resection with improved or preserved function

49
Q

When to use radiation with meningiomas?

A

If symptomatic and not amenable to aggressive resection, significant residual tumor, recurrent tumor or newly diagnosed atypical or anaplastic meningioma

50
Q

Most important prognostic factor of meningioma

A

Extent of initial resection and histological tumor grade (recurrence free survival in some after total resection)

51
Q

When does outcome improve for meningioma and incomplete resection?

A

If post op radiation

52
Q

What is primary CNS lymphoma?

A

Rare and aggressive extra nodal non hodgkin lymphoma

53
Q

When do you see more primary CNS lymphomas?

A

HIV infection (EBV) and organ transplant recipients

54
Q

How are most primary CNS lymphomas classified

A

Diffuse large cell B lymphoma

55
Q

Presentation of primary CNS lymphoma

A

AMS and focal neuro sxs
Deficits progress rapidly and diagnose in 2-3 mos
Less seizures than with gliomas
Can have lymphomatous infiltration, leptomeningeal dissemination

56
Q

What does primary CNS lymphoma have predilection for?

A

Deep or midline brain structures

57
Q

MRI for primary CNS lymphoma

A

Multifocal lesions that are bright with homogenous contrast enhancement in half of pts

58
Q

Therapy for primary CNS lymphoma

A

Corticosteroids reduce peritumoral edema and have direct oncolytic effect to have temporary improvement (steroids should be held prior to biopsy since it might make it nondiagnostic)

59
Q

What is no longer recommended for newly diagnosed primary CNS lymphoma

A

Whole brain RT (inadequate control with high tumor recurrence and neurotoxicity)

60
Q

Standard initial induction therapy for newly diagnosed primary CNS lymphoma

A

High dose methotrexate

61
Q

What might high dose methotrexate cause?

A 
Delated leukoencephalopathy (progressive dementia, gait disturbance)
-risk increased when pt gets MTX during or after RT
62
Q

What therapy might be considered for younger pts with good performance with primary CNS lymphoma?

A

Intensive chemo followed by autologous stem cell transplantation without whole brain radiation

63
Q

Most common embryonal brain tumor in children

A

Medulloblastoma

64
Q

Where see medulloblastoma in kids?

A

In or near cerebellar vermis and fourth ventricle (adults are above)

65
Q

First line tx for medulloblastomsa

A

Surgery (gross total resection)

66
Q

Sxs of medulloblastoma

A

HAs, vomiting (AM), lethargy, gait ataxia

Likely to disseminate and metastasize outside CNS

67
Q

Presentation of medulloblastoma in cerebellar hemisphere

A

Ipsilateral ataxia w/ or without signs of increased ICP

68
Q

Presentation of medulloblastoma in brainstem

A

Cranial nerve palsies and long tract finding (spasticity, hyperreflexia)

69
Q

Medulloblastoma on MRI

A

Homogenously or heterogenously enhancing mass that fills or distorts fourth ventricle
Calcifications or hemorrhage
Hydrocephalus

70
Q

How to classify medulloblastoma into prognostic groups

A

Extent of initial surgical resection
Presence/absence of leptomeningeal dissemination at diagnosis
CSF cytology

71
Q

Tx failure of medulloblastoma

A

Commonly due to recurrence in posterior fossa with or without leptomeningeal dissemination

72
Q

Tx for high risk children with medulloblastoma

A

Multiagent chemo during and after standard radiation improves survival

73
Q

Where does ependyoma come from?

A

Ependymal cells which line ventricles and central canal
More common in kids
*fourth ventricle mostly

74
Q

Common presentation of ependymoma

A

Hydrocephalus and increased ICP

75
Q

Most common type of brain tumor

A

Metastatic tumors

76
Q

Where do metastatic tumors tend to go to in the brain?

A

Gray white matter junction in middle cerebral artery terriotry

77
Q

Order of frequency of metastatic tumors

A 
Lung (lots of non small cell lung cancer pts have them)
Breast
Melanoma
Renal
GI tumors
78
Q

Signs of malignancy

A 
Cachexia
Lymphedema
Asymmetric breath sounds
Breast mass
Skin lesions
79
Q

Clinical manifestations of CNS tumors

A 
Increased ICP:
HA (nocturnal or worse in morning, aggravated by coughing, valsalva maneuver or postural change)
Nausea
Papilledema
AMS
False localizing signs (CN IV palsy)
80
Q

Causes of increased ICP with metastatic tumors

A

Mass effect from tumor
Surrounding edema
Hemorrhage
Hydrocephalus

81
Q

Very common initial presentation of metastatic tumors

A

Seizures (partial with secondary generalization-temporal lobe tumors)

82
Q

Most common presentation of cerebral hemispheric tumors

A

Seizures

83
Q

Presentation of tumors in posterior fossa

A

Ataxia and cranial serve signs

84
Q

Presentation of tumors in ventricles or near cerebral aqueduct

A

Signs of increased ICP

85
Q

Presentation of tumors in spinal cord

A

Paraparesis, sensory loss, urinary incontinence

86
Q

Why is CT scan helpful with tumors?

A

Bone involvement

87
Q

What is always started with tumors to decrease mass effect and surrounding edema?

A

Corticosteroid (dexamethasone)

88
Q

Relative contraindication for tPA

A

Brain tumors

89
Q

Tx of VTE with tumors

A

Low molecular weight heparinoids

X Clin Med III Exam 3 (7 decks)

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