M6 L6: Antineoplastics Flashcards

1
Q

what is neoplasm

A

abnormal tissue growth
- types: malignant, benign

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2
Q

what are malignant tumors

A
  • cancer
  • tends to spread
  • may affect any tissue, too many types

3 main characters (this is what makes fighting cancer hard):
- proliferation
- invasion
- metastasis

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3
Q

3 main classes of cancer

A
  1. carcinoma (epithelial cells)
  2. sarcoma (non-epithelial cells)
  3. lymphoma and leukemia (hematopoietic)
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4
Q

what are the main 3 cancer treatments

A
  • surgery
  • radiation
  • chemotherapy (antineoplastics)
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5
Q

general indications of antineoplastics

A
  • combined w surgery and/or radiotherapy
  • inoperable tumor
  • no response to radiotherapy
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6
Q

what should you monitor with antineoplastics

A

CBC - liver - renal functions

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7
Q

why is it useful to combine antineoplastics

A
  1. attack cells by diff mechanisms bc these cells are the most aggressive you will see
  2. when you use combo therapy these drugs are very nasty, and very aggressive on the body
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8
Q

adverse effects of antineoplastics

A

(LITERALLY ANYTHING CAN BE AN ADVERSE EFFECT)
- alopecia
- bone marrow suppression (anemia, infection, bleeding)
- cardiac stuff
- GI stuff
- hepatotoxic, nephrotoxic, neurotoxic
- teratogenic
- cytotoxic, mutagenic

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9
Q

what are the major classes of antineoplastics

A
  • antimetabolites
  • antimitotics
  • alkylating agents
  • topoisomerase inhibitors
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10
Q

what do antimitotics (these interfere with mitosis) target

A

metaphase

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11
Q

what do antibiotics target

A

anaphase, early protein synthesis

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12
Q

what does alkylating agents

A
  • DNA synthesis
  • metaphase
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13
Q

what do antimetabolites target

A

DNA synthesis

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14
Q

what are antimetabolites

A

chemotherapy drug bc they kill cells

  • analogues of normal cell metabolites (ex: purines, and pyrimidines bases)
  • interfere with structure of the nucleic acids, they have a structure that is similar but not identical, the value of this is to interfere w structure of DNA and replace these bases, like undercover bc they will not work which is good bc it won’t function and will end up being destroyed
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15
Q

in RNA what is thymine replaced as

A

uracil

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16
Q

mechanism of action for antimetabolites

A
  • competitive decrease of the metabolites interfere with DNA and RNA synthesis
  • they stop growth and division of malignant cells
  • does this during “S” phase of interphase
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17
Q

what is S phase

A

the time where you synthesis DNA to build up the other set of DNA for cell division
* so perfect time for these drugs to work

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18
Q

classes of antimetabolites

A
  1. purine analogues (6-mercaptopurine 6-MP)
  2. pyrimidine analogues (5-fluorouracil 5-FU, cytosine arabinoside [cytarabine])
  3. antifolates (methotrexate
19
Q

mech of action for methotrexate

A
  • folic acid analogue:
    decreases DHFR enzyme -> decreases THF (which is essential for purine and pyrimidine bases)

(inhibits folic acid, which is important for DNA and RNA synthesis)

20
Q

indications for methotrexate

A
  • cancer chemo
  • autoimmune diseases
21
Q

how do you administer methotraxate

A

oral, parenteral

22
Q

what does trimethoprim attack

A

bacteria

23
Q

what does methotrexate attack

A

our cells

24
Q

which would have worse adverse effects:
1. trimethoprim
2. methotrexate

A

2

25
Q

what are antimitotics

A
  • plant alkaloids
  • target the mitotic (M) phase of cell cycle
26
Q

main types of antimitotics

A
  1. vinca alkaloids
    ex: vincristine and vinblastine
  2. Taxanes
    ex: paclitaxel (taxol)
27
Q

what are microtubules

A
  • tubulin protein polymers
  • mandatory for cell division
28
Q

mech of action for antimitotics

A

they will bind to tubulin which
- vinca alkaloids: decreases polymerization -> preventing microtubule formation
- taxanes: stabilize microtubules -> prevent separation of chromosomes

29
Q

what do alkylating agents do

A
  • add alkyl group to DNA by covalent bond
  • this causes DNA damage and cell death because strands are unable to uncoil (because of added cross links to DNA strands) and because of abnormal base-pairing
30
Q

types of alkylating agents

A
  1. nitrogen mustards (ex: cyclophosphamide, chlorambucil)
  2. nitrosoureas (ex: carmustine)
  3. platinum-based drugs - alkylating like agents (ex: cisplatin)
31
Q

what are topoisomerases

A
  • nuclear enzymes
  • modulate DNA topology (by unwinding and winding DNA strands, required for mRNA transcription and DNA replication)
32
Q

what is topoisomerase 1

A

cut and ligate single strand of DNA

33
Q

what is topoisomerase 2

A

cut and ligate both strands of DNA

34
Q

what is the action of topoisomerase inhibitors

A

blocks DNA ligation -> DNA breaks -> interrupt protein synthesis & cell division -> apoptosis (process of programmed cell death)

35
Q

what is an example of topoisomerase 1 inhibitors

A

irinotecan

36
Q

what are topoisomerase 2 inhibitors

A
  1. antineoplastics (ex: doxorubicin, etoposide)
  2. antibiotics: quinolones (inhibit bacterial topoisomerase 2 [DNA gyrase])
37
Q

what do antitumor antibiotics in treatment of tumors

A
  • interfere with RNA and DNA synthesis -> interrupt tumor cell growth and reproduction
    ex: actinomycin - bleomycin
38
Q

what do hormones do for treatment of tumors

A
  • selective suppression of tumor cells
    ex: steroids, tamoxifen (anti-estrogen)
39
Q

what do retinoids do in treatment of tumors

A
  • vit A analogues - stim apoptosis
    ex: fenretinide
40
Q

what do antiangiogenic agents do to treat tumors

A

interfere w neovascularization - interrupt tumor growth and spread

41
Q

for breast cancer what can you combine for chemo

A

doxorubicin (Ti-2 decrease) + cyclophosphamide (alkyl agent) +/- taxol (antimitotic)

42
Q

what combo should you use for acute lymphoblastic leukemia

A

vincristine (antimitotic) + dexamethasone (steroid) + asparaginase (hydrolytic enzyme)

43
Q

what combo should you use for hodgkin lymphoma

A

cyclophosphamide + vincristine + prednisone + procarbazine hydrochloride