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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
Imaging of low grade gliomas
Poorly circumscribed lesions with diffuse infiltration | Hard to define gross and microscopic margins
26
What might help the diagnostic accuracy with low grade gliomas?
Tumor debulking
27
Which is more sensitive to chemo: oligodendrogliomas or astrocytomas
Oligodendrogliomas (has better prognosis too)
28
Where does oligodendroglioma originate?
Oligodendrocytes (produce myelin sheaths in CNS) | -low and high grade types
29
Classic histological features of oligodendrogliomas
Uniform round nuclei and clear perinuclear halos (fried egg) with network of branching capillaries (chicken wire)
30
Classification of most oligodendrogliomas
Most have 1p/19q co deletion (may also have TP53 mutation)
31
MRI for low grade astrocytoma
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
32
How does low grade oligodendroglioma look on MRI?
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)
33
Younger pt with oligodendrogliomas and no neuro sxs
Defer surgery/RT (not negative impact if do so)
34
Why to prolong radiation as long as possible?
Can cause neurotoxicity
35
When to give radiation to pt with oligodendrogliomas?
Not candidate for aggressive tumor resecti on Have large post op tumor burden >50 YO at diagnosis
36
Indications of early intervention with oligodendroglioma and astrocytoma
Neuro sxs other than seizures Presence of significant mass effect on imaging Growth of lesion on serial scans Age >50
37
Prognosis of astrocytoma
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
What is present in most newly diagnosed low grade oligodendrogliomas
1p/q19 co deletion
39
Importance of 1p/q19 co deletion with oligodendroglioma
Independent prognostic marker for less aggressive behavior, better response to tx (chemo) and better overall survival
40
Where does meningioma come from?
Arachnoid cells
41
Presence of meningioma
``` Most asymptomatic (found on imaging or autopsy) Symptomatic twice as comon in women (estrogen and progesterone receptors on tumor) ```
42
Imaging for meningioma
Encircle on another, forming calcified whorls called psammoma bodies (solitary contrast enhancing lesions adjacent to dural surfaces)
43
Classification of meningiomas
Grade 1: most and best to have Grade 2: atypical and diagnosis made on brain invasion Grade 3: malignant/anaplastic
44
Common sites of origin for meningiomas
Cerebral convexity, parasagittal area, falx and sphenoid ridge
45
Presentation of meningioma
Slow growth with slow progression of sxs Hyperostosis in skull adjacent to tumor and this bone usually invaded by tumor cells Peritumor edema
46
Imaging for meningioma
MRA/MRV to determine blood supply in consideration for surgery or preop embolization
47
Can you use chemo for meningiomas?
Not sensitive
48
Therapy for meningioma
Defer tx until sxs develop or tumor enlarges | Symptomatic: total surgical resection with improved or preserved function
49
When to use radiation with meningiomas?
If symptomatic and not amenable to aggressive resection, significant residual tumor, recurrent tumor or newly diagnosed atypical or anaplastic meningioma
50
Most important prognostic factor of meningioma
Extent of initial resection and histological tumor grade (recurrence free survival in some after total resection)
51
When does outcome improve for meningioma and incomplete resection?
If post op radiation
52
What is primary CNS lymphoma?
Rare and aggressive extra nodal non hodgkin lymphoma
53
When do you see more primary CNS lymphomas?
HIV infection (EBV) and organ transplant recipients
54
How are most primary CNS lymphomas classified
Diffuse large cell B lymphoma
55
Presentation of primary CNS lymphoma
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
What does primary CNS lymphoma have predilection for?
Deep or midline brain structures
57
MRI for primary CNS lymphoma
Multifocal lesions that are bright with homogenous contrast enhancement in half of pts
58
Therapy for primary CNS lymphoma
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
What is no longer recommended for newly diagnosed primary CNS lymphoma
Whole brain RT (inadequate control with high tumor recurrence and neurotoxicity)
60
Standard initial induction therapy for newly diagnosed primary CNS lymphoma
High dose methotrexate
61
What might high dose methotrexate cause?
``` Delated leukoencephalopathy (progressive dementia, gait disturbance) -risk increased when pt gets MTX during or after RT ```
62
What therapy might be considered for younger pts with good performance with primary CNS lymphoma?
Intensive chemo followed by autologous stem cell transplantation without whole brain radiation
63
Most common embryonal brain tumor in children
Medulloblastoma
64
Where see medulloblastoma in kids?
In or near cerebellar vermis and fourth ventricle (adults are above)
65
First line tx for medulloblastomsa
Surgery (gross total resection)
66
Sxs of medulloblastoma
HAs, vomiting (AM), lethargy, gait ataxia | Likely to disseminate and metastasize outside CNS
67
Presentation of medulloblastoma in cerebellar hemisphere
Ipsilateral ataxia w/ or without signs of increased ICP
68
Presentation of medulloblastoma in brainstem
Cranial nerve palsies and long tract finding (spasticity, hyperreflexia)
69
Medulloblastoma on MRI
Homogenously or heterogenously enhancing mass that fills or distorts fourth ventricle Calcifications or hemorrhage Hydrocephalus
70
How to classify medulloblastoma into prognostic groups
Extent of initial surgical resection Presence/absence of leptomeningeal dissemination at diagnosis CSF cytology
71
Tx failure of medulloblastoma
Commonly due to recurrence in posterior fossa with or without leptomeningeal dissemination
72
Tx for high risk children with medulloblastoma
Multiagent chemo during and after standard radiation improves survival
73
Where does ependyoma come from?
Ependymal cells which line ventricles and central canal More common in kids *fourth ventricle mostly
74
Common presentation of ependymoma
Hydrocephalus and increased ICP
75
Most common type of brain tumor
Metastatic tumors
76
Where do metastatic tumors tend to go to in the brain?
Gray white matter junction in middle cerebral artery terriotry
77
Order of frequency of metastatic tumors
``` Lung (lots of non small cell lung cancer pts have them) Breast Melanoma Renal GI tumors ```
78
Signs of malignancy
``` Cachexia Lymphedema Asymmetric breath sounds Breast mass Skin lesions ```
79
Clinical manifestations of CNS tumors
``` 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
Causes of increased ICP with metastatic tumors
Mass effect from tumor Surrounding edema Hemorrhage Hydrocephalus
81
Very common initial presentation of metastatic tumors
Seizures (partial with secondary generalization-temporal lobe tumors)
82
Most common presentation of cerebral hemispheric tumors
Seizures
83
Presentation of tumors in posterior fossa
Ataxia and cranial serve signs
84
Presentation of tumors in ventricles or near cerebral aqueduct
Signs of increased ICP
85
Presentation of tumors in spinal cord
Paraparesis, sensory loss, urinary incontinence
86
Why is CT scan helpful with tumors?
Bone involvement
87
What is always started with tumors to decrease mass effect and surrounding edema?
Corticosteroid (dexamethasone)
88
Relative contraindication for tPA
Brain tumors
89
Tx of VTE with tumors
Low molecular weight heparinoids

X Clin Med III Exam 3 (7 decks)

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