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Pharmacology > Exam 50- Antineoplastic > Flashcards

Exam 50- Antineoplastic Flashcards

1
Q

tumor initiation and progression

A
  1. genetic mutation leads to abnormal proliferation
  2. more mutations occur within cells
  3. advantageous mutations are selected so tumor becomes increasing malignant
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2
Q

___ cells before cancer is identified

A

10 billion

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3
Q

adverse affects of antineoplastic drugs to blood

A

anemia (low RBC)
thrombocytopenia (low platelet)
leukopenia (low WBC)

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4
Q

adverse affects of antioplastic drugs to the GI

A 
nausea
vomiting
diarrhea
anorexia
mucositis
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5
Q

other advers affects of antioplastic drugs

A

opportunistic infections
alopecia (hair cells)
teratogenesis
secondary cancers

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6
Q

rationale for combined therapy

A
  1. decreased resistance
  2. increase tolerability
  3. increase efficacy
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7
Q

combination therapy combines drugs with different:

A

MOA
cell cycle phase activity
dose-limiting toxicity

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8
Q

Hodgkin’s Lymphoma combination therapy

A 
ABVD
A=doxorubicin (G2)
B=bleomycin (G2)
V=vinblasine (M)
D=dacbazine (G1 and S)
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9
Q

G1 phase

A

prep for DNA replicatin

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10
Q

S phase

A

DNA replication

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11
Q

G2 phase

A

prep for mitotis

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12
Q

M phase

A

=Mitosis

separate of daughter chromosomes and cell division

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13
Q

Check points of Cell Cycle

A
  1. DNA damage checkpoint- in G1
    - detects damage before entering S as DNA’s being synthesized
  2. Spindle checkpoints - in M
    detect any failure of spindle fibers to form properly
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14
Q

Phase specific drugs general

A
  • most active at a particular phase of the cell cycle
  • time dependent!!
  • more effective against tumors exhibiting log growth pattern
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15
Q

phase non-specific drugs

A
  • exert toxic effects on cell during cycle, but not a specific part
  • effective in both high and low growth fraction tumors
  • concentration dependent!! ∴ give highest dose tolerable
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16
Q

DNA Damaging Agents

A
  1. Alkylating agents

2. Antitumor antibiotics

17
Q

alkylating agnets

A

dacarbazine

  • covalently couples alkyl groups to nucleophillic sites on DNA =APOPTOSIS
  • phase non-specific although peak at late G1 and S phases
  • mutagenic, carcinogenic
18
Q

antitumor antibiotics

A 
phase-nonspecivic: although cell is arrested in G2
doxorubicin
-binds to and inhibits DNA function
bleomycin
-binds to DNA and causes free radicals
19
Q

doxorubicin MOA

A

binds to DNA and prevents strand passage and relegation (joining) by topoisomerase II

20
Q

bleomycin MOA

A

binds to DNA and chelates Fe
-accumulates free radicals

also causes pulmonary fibrosis

21
Q

Microtubule function inhibitors

A

vinca alkaloids
(and taxanes)

M phase specific

22
Q

vinca alkaloids

A

vinblasitne

  • bind to alpha and beta tubulin
  • prevents spindle formation and leads to an inability of cells to secrete chromosomes and cell death
23
Q

Inhibitors of DNA Synthesis (types)

A

folate synthesis inhibitors
antimetabolites
topoisomerase inhibitors

Phase S specific

24
Q

antimetabolites

A

purine antagonists
=thioguanine
pyrimidine antagoinsts

MOA= insert into DNA and cause
chain termination
strand breakage
inhibition of cell growth

phase S

25
Q

folate analogues

A

methotrexate

  • inhibits dihydrofolate reductase
    • this enzyme converts dihydrofolate to tetrahydrofolate and eventually into purines

treatment=
lethal dose of methotrexate followed by foiling acid
-rescues cells less dependent on purine synthesis

S phase

26
Q

topoisomerase inhibitors

A

topotecan

  • S phase specific
  • inhibits topoisomerase I

active in S phase

27
Q

topoisomerase I

A

unravels DNA helix for replication

28
Q

primary resistance to chemotherapy

A
  1. mutations of p53
    - enzyme that shunts to apoptosis, if mutated won’t catch alkylation
  2. compromised mismatch repair enzyme family
    - enzymes that repair problems with nicked strands, mismatched DNA or chain termination are compromised os they don’t send cell to programmed cell death
29
Q

acquired resistance to chemotherapy

A

due to drug use, not inherent to cancer

  1. resistance to specific drug
    -reduced drug uptake, or drug deactivation
  2. broad resistance to many drugs
    =increased MDR1 expression
    -codes a cell surface protein that enhances drug efflux form cell
30
Q

bevacizumab

A
  • antiangiogenic
  • inhibit tumor blood vessel growth
  • targets vascular endothelial GF
  • monoclonal antibody ∴ immunotherapy
31
Q

tamoxifen

A

=Selective Estrogen Receptor Modulator (SERM)
1. antagonist to ER in breast
=inhibits growth-promoting proteins ∴ breast cancer
2. partial agonist to ER in endometrium
=increases risk for endometrial cancer

32
Q

Hep B cancer

A

=DNA virus

associated with liver cancer

33
Q

HPV cancer

A

=DNA virus

associated with cervical cancer

34
Q

Herpesviruses cancer

A

=DNA Virus
associated with Burkitt’s lymphoma
Kaposi’s sarcoma
nasopharyngeal carcinoma

35
Q

Hep C cancer

A

=RNA virus

associated with liver

36
Q

Retrovirus cancer

A

=RNA virus

associated with adult T-cell leukemia

37
Q

Gardasil

A

prevents infection from HPV types 6, 11, 16, and 18

16 and 18 -> cervical cancer
6 and 11 -> genital warts

38
Q

oncogenes

A

genes that promote cell proliferation and inhibit programmed cell death
-if mutated or over expressed = mitosis

normal cells require growth factors, but mutations result in growth factor independence

39
Q

imatinib

A

=Kinase inhibitor

BCR-ABL gene => fusion protein (continuously active kinase)

-imatinib = 50-95% of puts with chronic myeloid tumor

Pharmacology (11 decks)

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