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Oncology Exam 1 > Qin- Cancer Chem > Flashcards

Qin- Cancer Chem Flashcards

1
Q

True or False: None of the chemotherapy drugs are cancer cell-specific. They are all simply quickly dividing cell specific.

A

True

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2
Q

True or False: the reason many chemotherapy drugs cause side effects such as nausea, myelosuppression, ulceration, and hair loss is because they target quickly dividing cells such as those in the bone marrow and in the gut.

A

True

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3
Q

True or False: Cyclophosphamide is a prodrug.

A

True

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4
Q

True or False: Cyclophosphamide is an alkylating agent that is well absorbed orally.

A

True

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5
Q

True or False: Cyclophosphamide is inactive until it is activated by enzymes in the kidney.

A

FALSE! It must be activated by liver enzymes.

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6
Q

Cyclophosphamide causes life threatening damage to the bladder due to ______, resulting in hemorrhagic cystitis.

A

Acrolein

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7
Q

In order to prevent hemorrhagic cystitis in patients taking cyclophosphamide, treat patients with _____, which is given simultaneously with the chemo drug.

A

MESNA

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8
Q

MESNA assists in detoxifying acrolein by reaction of its sulfhydryl group with an unsaturated carbon group to neutralize it. This reaction is known as the _____ addition.

A

Michael

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9
Q

______ and _____ are nitrosourea alkylating agents that are able to cross the BBB due to their high degree of lipophilicity. Therefore, they’re used in the treatment of brain tumors.

A

Carmustine and lomustine

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10
Q

Carmustine (BCNU) adds a chloroethyl group to guanine and thus damages the DNA. If a cancer cell has a high expression of the _____ enzyme, it can repair the DNA base and therefore cause carmustine resistance.

A

O6-AGAT

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11
Q

True or False: Platinum compounds (cisplatin, carboplatin, oxaliplatin) are stable in an aqueous environment.

A

FALSE! They are unstable and become reactive.

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12
Q

The sensitivity of testicular tumors to cisplatin is attributed to the abundant expression of _________ domain proteins in the testes. These proteins bind to the crosslinks induced by cisplatin, blocking recognition of these lesions by nucleotide excision repair (NER) enzymes, as well as preventing replicative bypass.

A

HMG (High Mobility Group)

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13
Q

_______ is a cytoprotective agent used in combination with cisplatin to protect the kidneys from nephrotoxicity. It can do this because the levels of alkaline phosphate are (lower OR higher) in normal tissues than neoplastic issues.

A

Amifostine

Higher in normal tissues than neoplastic tissue.

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14
Q

Combining cisplatin with (Hypotonic OR normal OR hypertonic) saline reduces its lethality and permits higher platinum doses to be given.

A

Hypertonic

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15
Q

True or False: Cisplatin is associated with N/V, renal damage, peripheral neuropathy, and ototoxicity.

A

True

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16
Q

True or False: Cisplatin is associated with myelosuppression.

A

FALSE! it is not myelosuppressive. Carboplatin is associated with myelosuppression.

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17
Q

The main adverse effect of oxaliplatin is ________.

A

Peripheral neuropathy

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18
Q

Triazine alkylating agents (dacarbazine and temozolamide) cause what type of modification to DNA?

A

DNA methylation

19
Q

Methotrexate falls under which antimetabolite class?
A. Folate antagonist
B. Pyrimidine analogue
C. Purine analogue

A

A. Folate antagonist

20
Q

Mercaptopurine falls under which antimetabolite class?
A. Folate antagonist
B. Pyrimidine analogue
C. Purine analogue

A

C. Purine analogue

21
Q

Cytarabine falls under which antimetabolite class?
A. Folate antagonist
B. Pyrimidine analogue
C. Purine analogue

A

B. Pyrimidine analogue

22
Q

Gemcitabine falls under which antimetabolite class?
A. Folate antagonist
B. Pyrimidine analogue
C. Purine analogue

A

B. Pyrimidine analogue

23
Q

Fluorouracil falls under which antimetabolite class?
A. Folate antagonist
B. Pyrimidine analogue
C. Purine analogue

A

B. Pyrimidine analogue

24
Q

Capecitabine falls under which antimetabolite class?
A. Folate antagonist
B. Pyrimidine analogue
C. Purine analogue

A

B. Pyrimidine analogue

25
Q

In general, antimetabolites are the most effective during the ____ phase of the cell cycle, when DNA synthesis is occurring at a maximal rate.

A

S cycle

26
Q

True or False: Antimetabolite agents are considered cell-cycle specific.

A

True

27
Q

Folic acid serves as a coenzyme in the biosynthesis of nucleic acid bases. The active form of folic acid is tetrahydrofolate, which is produced by the enzyme ________. Methotrexate serves as an inhibitor of this enzyme and therefore causing a deficiency of folate coenzymes and inhibiting thymidine synthesis.

A

Dihydrofolate reductase (DHFR)

28
Q

True or False: By shutting down DHFR methotrexate is an inhibitor of nucleoside/nucleotide biosynthesis.

A

True

29
Q

______, a folate antagonist, is useful in the treatment of psoriasis and rheumatoid arthritis.

A

Methotrexate

30
Q

The receptor responsible for getting folate into the cell is called _____, and the receptor responsible for getting anti-folate compounds, such as methotrexate, and reduced folates, such as leucovorin, into the cell is called _________.

A

Folate receptor

Reduced folate carrier type 1

31
Q

The attachment of __________ to folate and anti-folate compounds may increase overall negative charge of the molecules, which will help trap either folic acid or anti-folate compounds into the cells to exert the biological function.

A

Glutamate

32
Q

____________ is given with methotrexate to rescue the normal cells. It is important not to confuse folinic acid with folic acid because the results can be fatal!

A

Leucovorin

33
Q

___________ is a recombinant form of carboxypeptidase G2 (a bacterial enzyme) that is used to reverse toxic levels of methotrexate in the system.

A

Glucarpidase

34
Q

_________ is a pyrimidine inhibitor that mimic uracil by attaching to a ribose then phosphorylated at the 5’ position to generate an intermediate of FdUMP – this intermediate is a potent inhibitor of Thrymidylate synthase, which blocks the synthesis of thymine.

A

5-fluorouracil

35
Q

5-fluorouracil is deactivated by ______.

A

DPD

36
Q

___________ mimics cytosine and is the standard care of AML. It is the most effective single agent for remission induction in AML.

A

Cytarabine

37
Q 
\_\_\_\_\_\_ is a pyrimidine analogue that works by 2 mechanisms: Inhibiting DNA synthesis and inhibiting ribonucleotide reductase (RNR).
A. Cytarabine
B. Gemcitabine
C. 6-mercaptopurine
D. 5-fluorouracil
E. Capecitabine
A

B. Gemcitabine

38
Q

Individuals who carry a variant of TPMT or lack the enzyme altogether can have high cellular concentrations of 6-thioguanine nucleotides and experience severe and sometimes fatal hematopoietic toxicity when given conventional doses of _________.

A

6-Mercaptopurine

39
Q

6-mercaptopurine is a substrate for ________, which is inhibited by allopurinol. Therefore, it is important to use lower doses of 6-MP when the patient is also on allopurinol.

A

Xanthine Oxidase (XO)

40
Q

True or False: Xanthine oxidase (XO) is found in high concentrations in milk, which is why 6-MP should not be taken with milk.

A

True

41
Q

Vinca alkaloids (vinblastine/vincristine/vinorelbine) act as microtubule (stabilizers OR destabilizers), while taxanes act as microtubule (stabilizers OR destabilizers).

A

Vinca alkaloids = Destabilizers

Texans = Stabilizers

42
Q

_____ interact with the central portion (or Vinca binding site) of the β-tubulin subunit and thus prevent polymerization into microtubules.
A. Vinca alkaloids
B. Taxanes

A

A. Vinca alkaloids

43
Q

_____ should NEVER be given intrathecally because of its devastating neurotoxic effect, which are almost always fatal.

A

Vincristine

44
Q 
DNA topoisomerases are nuclear enzymes that reduce supercoiled DNA torsional stress, allowing selected regions of DNA to become sufficiently untangled and relaxed to permit replication, recombination, repair, and transcription to occur. Topoisomerases are classified as type I and type II. Type I enzymes cleave one DNA strand and type II cleave both strands to perform their catalytic functions. Which of the following is NOT a topoisomerase II inhibitor?
A. Etoposide
B. Daunorubicin
C. Topotecan
D. Doxorubicin
E. Mitoxantrone
A

C. Topotecan

Oncology Exam 1 (5 decks)

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