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Pharm Exam 4 > Chemo Exam 4 Pharm > Flashcards

Chemo Exam 4 Pharm Flashcards

1
Q

What is Herceptin

A

It is a Her2 specific antibody for Tx of Breast Cancer

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2
Q

What occurs in the G phases of the Cell Cycle

A

RNA and Prot Synthesis

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3
Q

What occurs in the S phase of the Cell Cycle

A

DNA duplication

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4
Q

What are the Cycle-Specific Agents?

A
  1. Alkylating Agents 2. Cytotoxic Abx 3. Platinum Derivatives
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5
Q

What ist he MOA of Alkylating Agents?

A

They form covalent bonds w/ DNA that denature it and impee DNA transcription and translation

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6
Q

What base is the main molecular target of the Alkylating agents?

A

Guanine

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7
Q

What are the Nitrogen Mustards

A

Cyclophsophamide, Ifosfamide+mesna, Chlorambucil, Mechlorethamine

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8
Q

How do nitrogen mustards work?

A

They intercalate into double DNA strands and crosslink DNA

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9
Q

What is a contraindication of cyclophosphamide?

A

It is activated by CYP450 oxidases so it cannot be used in liver deficient pts

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10
Q

What is a major toxicity of cyclophosphamide and how can it be overcome?

A

Hemorrhagic cystites due to acrolein (metabolite), can help if drink lots of H2O to pee it off

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11
Q

What is Mechlorethamine used for?

A

Tx Hodgkin’s Disease

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12
Q

What alkylating agents can go through the BBB?

A

Nitroso-ureas

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13
Q

What is a major toxicity of Doxorubicine?

A

Cummulative cardiotoxicity leading to arrhythmias and HF

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14
Q

What is Cisplatin?

A

Water-soluble planar coordination complex w/ 2 Cl- and 2 NH3 groups

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15
Q

MOA of Cisplatin?

A

Interstrand and Intrastrand Cross-linking; Causes H-bond breaking b/w guanine and cytosine

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16
Q

What are good uses of Cisplatin?

A

Testicular and ovarian cancers

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17
Q

What are the S-Phase Specific Agents?

A
  1. Antimetabolites 2. Etoposide 3. Hydroxyurea
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18
Q

What is the MOA of S-phase Specific Agents?

A

Block metabolic PW involved in DNA Synthesis

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19
Q

What enzyme does Methotrexate Inhibit?

A

Dihydrofolate reductase and also Thymidylate synthase

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20
Q

What is MOA of 5-FU

A

Incorporated into mRNA and inhibits Thymidilate synthetase activity to inhibit DNA synthesis

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21
Q

What is the MOA of Etoposide?

A

Induces stable DNA double strand breaks by inhibiting topoisomerase II activity

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22
Q

What phase of the cell cycle does Etoposide inhibit?

A

S-G2 Transition

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23
Q

What is the MOA of M phase Specific Agents?

A

Poisons of the mitotic spindle

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24
Q

What are the M phase Specific Agents?

A
  1. Vinca alkaloids 2. Taxanes 3. Epothilones
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25
Q

What 2 M-phase specific cmpds inhibit Microtubule growth and tubulin polymerization?

A

Vincristine and Vinblastine

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26
Q

What is an expected toxicity of Vincristine?

A

Peripheral Neurotoxicity

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27
Q

What is the MOA of Taxanes?

A

Stabilize MTs in their polymerized state

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28
Q

What are the 3 benefits of Epothilones over Taxanes?

A
  1. Easier to synthetically modify 2. Poor substrate for P-glycoprotein 3. High affinity for beta-tubulin isoforms
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29
Q

What is the MOA of Arsenic Trioxide?

A

Induces degredation of PML-RARalpha in APML; and Downregulates Bcr-Abl in CML

30
Q

What is the ending for the Tyr Kinase inhibitors?

A

Inib

31
Q

What is the MOA of Rapamycin?

A

It inhibits the mTOR pw

32
Q

What is Tamoxifen?

A

It is a selective estrogen receptor modulator

33
Q

What is the MOA of Tamoxifen?

A

Competitive Estrogen Receptor Antagonist

34
Q

What are the Most Common distressing early toxic effects of Chemo

A

Nausea and Vomiting

35
Q

What is the major problem w/ chemotherapy?

A

Cell subpopulations can be compartmentalized into dividing cells, temporarily nondividing cells, and permanently nondividing cells

36
Q

Define Cure

A

Absence of disease resurgence during normal life expectancy

37
Q

What are some barriers to chemo?

A
  1. Hypoxic Cells 2. Drug Resistance 3. Low growth fraction 4. Advanced Tumor 5. Immunoincompetence
38
Q

What is the log kill hypothesis?

A

A given dose kills a constant proportion of cell population and not number of cells. This means can never get to zero with chemo alone

39
Q

What can Alkylating agents do at high doses?

A

Kill cells in G0 phase; any drug that can kill in G0 will be highly toxic to bone marrow and immune system

40
Q

What are the indications for Cyclophosphamide?

A

Broad spectrum

41
Q

What is Mesna?

A

It is a sulfhydryl reagent w/ uroprotective effects

42
Q

What is the drug of choice for Chronic lymphocytic leukemia?

A

Chlorambucil

43
Q

What is the MOA of Nitroso-Ureas?

A

They breakdown to form alkylating and carbamoylating compounds that bind to lysine residues and inactivate DNA repair enzymes

44
Q

What is the MOA of Doxorubicine

A

Stabilizeds Topoisomerase II so the DNA swivels and seizes up resulting in a DNA break

45
Q

What is important about the dosing of the Cytotocix Abx?

A

They have cumulative toxicity so one must consider total toxic dose

46
Q

What is the MOA of Bleomycin?

A

Metal chlating glycopeptide Abx that degrades DNA causing chain fragmentation and release of free bases

47
Q

Where is Bleomycin most effective?

A

G2 and M phases but also can act in G0

48
Q

What is the major toxicity w/ Bleomycin?

A

Pulmonary fibrosis (don’t use in pts w/ pulmonary insufficiency)

49
Q

What are the major toxicities of Cisplatin?

A

Nephrotoxic and GI distress

50
Q

What drug has a dose schedule based on the circadian rhythm?

A

Oxaliplatin

51
Q

How does methotrexate cause cell death?

A

It ultimately inhibits thymidylate synthesis

52
Q

What is Capecitabine?

A

It is a prodrug for 5-FU and is converted to active by thymidine phosphorylase

53
Q

What is the single agent in pts w/ breast cancer resistant to conventional therapy?

A

Capecitabine

54
Q

What cells quickly localize vinca alkaloids?

A

WBCs and plts

55
Q

What drug was 1 of the most important breakthroughs in chemo tx for breast cancer

A

Taxanes

56
Q

What are the indications for using taxanes?

A

Breast and ovarian cancers

57
Q

What is the most important toxicity of taxanes?

A

Peripheral neuropathy

58
Q

When is DNA Methyl transferase inhibitors the first line of defense?

A

Pts. w/ AML who are not candidates for intesnsive chemotherapy

59
Q

What are 2 problems w/ Tamoxifen?

A

Rapid resistance and Endometrial cancers

60
Q

What is Raloxifene?

A

It is an aromatase inhibitor to block steroid synthesis

61
Q

What is anastrozole?

A

It is an aromatase inhibitor to block steroid synthesis

62
Q

What are 2 risks of aromatase inhibitors?

A

Inc. bone turnover and Ultimately resistance

63
Q

What part of the brain mediates emesis?

A

The Chemoreceptor Trigger Zone of the medulla

64
Q

How is promethazine used to tx emesis resulting from chemo?

A

It blocks dopamine receptors in the CTZ

65
Q

What is the function of ondansetron and tropisetron?

A

They antagonize serotonin receptors in the CTZ

66
Q

What is the major side effect of cycle nonspecific drugs?

A

Hematologic toxicity of the primitive pluripotent stem cell lines

67
Q

What is radiation recall rxn?

A

When a drug causes an inflammatory rxn in tissue previously exposed to radiotherapy

68
Q

What medication has mandatory premedication for all pts?

A

Taxol b/c need to prevent hypersensitivity rxns

69
Q

What is a newer way to try to limit toxicity for specific organ?

A

Target specific tumors by formulating drugs combined w/ a liposomal carrier

70
Q

What is the major reason for anticancer failure?

A

Chemoresistance

71
Q

What is the primary goal of combination chemo?

A

Employ different modes of action to diminish resistance and high grade toxicity

72
Q

How do antisense DNA cancer tx work?

A

The antisense DNA drug binds to the mRNA and prevents translation

Pharm Exam 4 (3 decks)

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