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Neuro > Sweatman Treatment of Brain Tumors > Flashcards

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

A

MGMT

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

A

MGMT

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
Q

CARMUSTINE ALSO CALLED

A

BCNU

26
Q

LOMUSTINE ALSO CALLED

A

CCNU

27
Q

NITROSUREAS

A

CCNU AND BCNU

LOMUSTINE AND CARMUSTINE

28
Q

indications for BCNU (carmustine)

A

astrocytoma
brain mets
malignant glioma
medulloblastoma

29
Q

indications for CCNU (Lomustine)

A

Malignant Glioma

30
Q

cause apoptosis activation by DNA alkylation

A

Carmustine and Lomustine

31
Q

additional benefit of carmustine

A

decomposition products carbamolyate proteins which inhibit DNA repair

32
Q

cross resistance with other alkylating products in CCNU and BCNU tx

A

uncommon

33
Q

works via DNA alkylaiton and carbaoylation of proteins (ninhibit DNA repair

A

carmustine

34
Q

main tissue affectd and side effects of systemic ceeNu and BicNU usage

A 
hematopoetic supression
pulmonary toxicity
endocrine dysfunction esp with irraadiation therapy
elevate LFTS
encephalopathy
seizures
35
Q

high lipophillic and non-ionized at physiologic pH

A

carmustine and lomustine

36
Q

alkyalting agent given orally

A

lomustine

37
Q

alkylating agent given parenterally

A

carmustine

38
Q

can be administered after surgical excision with a long acting wafer formulation at the primary site–> thus mitigating systemic toxicity

A

carmustine

39
Q

gliadel-carmustine wafer-indicated for

A

high grade glioma

40
Q

convection enhanced delivery

A

instillation of a catheter and infusion under pressure of chemo agen which will diffuse into the tumor and surrounding tissue

41
Q

Chemo therapy related cognitive impairment AKA

A

chemo-fog

42
Q

mechanism for CRCI

A

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
Q

TNFalpha and CRCI can be blocked by

A

anti-tnfalpha antibodies

Neuro (19 decks)

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