Sweatman Treatment of Brain Tumors Flashcards

1
Q

most common tumor in brain

A

mets to brain from other primary site

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2
Q

mets to brain in what order

A

lung> breast>unknown>MELANOMA (high propensity)> renal

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3
Q

80% of brain mets occur in what part

A

cerebral hemispheres

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4
Q

15% OF BRAIN METS OCCUR INTO

A

cerebellum

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5
Q

5% of mets to brain occur into

A

brain stem

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6
Q

therapies to treat brain mets may also be more than just antitumorals

A

steroids to combat edema

anticonvulsants (to combat seizure but not until symptomatic)

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7
Q

DEFINITIVE TREATMENT OF BRAIN CA

A

SURGERY
WHOLE BRAIN RADIATION
RADIOSURGERY

*ALONE OR IN COMBO

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8
Q

T1 MODALITY

A

WATER IS dark

Fat is bright
contrast is white (hyperintense)

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9
Q

T2 modality

A

fat is intermediate bright

water is bright

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10
Q

t2 flair

A

stagnant water is bright

moving water is dark

but double check this shit

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11
Q

routine use of conventional chemo for brain mets….

A

no strong evidence for support

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12
Q

if you are going to use conentional chemo for brain mets…

A

need a BBB penetrating drug that reaches neuronal tissue in cytotoxic concentrations a(such as temozolomide) and WBRT (whole brain radiation therapy

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13
Q

astrocytes and tumor cells connected via

A

gap junctions

thus resistance to chemo ca come about not only by mechanisms within the tumor cell but also by gene-related effects produced by the astrocyte

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14
Q

key defining feature of CNS tumor resistance mechanisms that cause treatment outcomes to vary from the same tumoral types treated in the periphery

A

Tumor cells congregate and interconnect with astrocytes-via gap junctions-they provide “prevailing survival signalling” through differences in gene expresssion in the astrocyte that are passed on to the cancer cell

thus jsut because a cytotoxic agent reaches the CNA in proper concentrations-it doesnt necessarily have to respond as it would to the exact same concentration in the periphery

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15
Q

non enzymatically activated prodrug yielding a DNA methylating agent

A

temozolimide

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16
Q

temozolimide MOA

A

PRODUCES DNA DAMAGE
methylating agent that inhibits DNZ replication

METHYLATION MUTES MOST DNA

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17
Q

MYELOSUPRESSANT, LEUKOPENIA, THROMBOCYTOPENIA

N/V CHILLS 1-3 HOURS AFTER THERAPY

A

TEMOZOLIMIDE

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18
Q

CATEGORY X

A

temozolimide

19
Q

labeled uses for temozolomide

A

astrocytoma

GBM (astrocytoma IV grade)

20
Q

off label recommendations for temozolomide

A

malignant glioma

malignant melanoma

21
Q

SUICIDE REPAIR ENZYME IN SOME CANCER CELLS

22
Q

ONE PATH OF RESISTANCE TO TMZ

A

UPREGULATION OF MGMT–> THE DAMAGED CELL REPAIRS THE DNA DAMAGE WE CAUSED BY ADMIN TMZ

23
Q

RESTORE 3D TOPOLOGY OF DNA ALLOWING CELL DIVISION TO CONTINUE

24
Q

WHY DOES TMX CAUSE DOSE DEPENDENT MYELOSUPRESSIVE EFFECTS

A

HEMOTOPEITIC CELLS LACK THE ABILITY TO BEEF UP MGMT IN RESPINCE TO DNA METHYLATION CAUSED BY TMZ

25
CARMUSTINE ALSO CALLED
BCNU
26
LOMUSTINE ALSO CALLED
CCNU
27
NITROSUREAS
CCNU AND BCNU | LOMUSTINE AND CARMUSTINE
28
indications for BCNU (carmustine)
astrocytoma brain mets malignant glioma medulloblastoma
29
indications for CCNU (Lomustine)
Malignant Glioma
30
cause apoptosis activation by DNA alkylation
Carmustine and Lomustine
31
additional benefit of carmustine
decomposition products carbamolyate proteins which inhibit DNA repair
32
cross resistance with other alkylating products in CCNU and BCNU tx
uncommon
33
works via DNA alkylaiton and carbaoylation of proteins (ninhibit DNA repair
carmustine
34
main tissue affectd and side effects of systemic ceeNu and BicNU usage
``` hematopoetic supression pulmonary toxicity endocrine dysfunction esp with irraadiation therapy elevate LFTS encephalopathy seizures ```
35
high lipophillic and non-ionized at physiologic pH
carmustine and lomustine
36
alkyalting agent given orally
lomustine
37
alkylating agent given parenterally
carmustine
38
can be administered after surgical excision with a long acting wafer formulation at the primary site--> thus mitigating systemic toxicity
carmustine
39
gliadel-carmustine wafer-indicated for
high grade glioma
40
convection enhanced delivery
instillation of a catheter and infusion under pressure of chemo agen which will diffuse into the tumor and surrounding tissue
41
Chemo therapy related cognitive impairment AKA
chemo-fog
42
mechanism for CRCI
cytotoxics promote peripheral release of TNFalpha in response to cellular damage TNFalpha can access BBB tnfALPHA damages mitochondria and produces ROS via glial cell related mechanisms
43
TNFalpha and CRCI can be blocked by
anti-tnfalpha antibodies