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Pharmacology > EXAM 3 - Oncology - Just the Stars - GANNAWAY > Flashcards

EXAM 3 - Oncology - Just the Stars - GANNAWAY Flashcards

1
Q

Cell-cycle specific

A

Chemotherapeutic agents that are only effective on high growth fraction cancer cells.

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2
Q

Cell-cycle nonspecific

A

Chemotherapeutic agents that are effective on both low growth fraction and high growth fraction cancer cells.

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3
Q

Growth Fraction

A

The fraction of cancer cells that are actively replicating (cycling) in the cell cycle.

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4
Q

When is chemotherapy the only treatment option?

A

cancer that is disseminated and not amenable to surgery and/or radiation

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5
Q

Adjuvant Chemotherapy

A

Supplemental chemotherapy that is given following surgery and/or radiation to eliminate undetected micrometastases.

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6
Q

Neoadjuvant Chemotherapy

A

Chemotherapy that is given prior to surgery and/or radiation to decrease the size of a solid tumor.

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7
Q

Maintenance Chemotherapy

A

continued after initial ﾓcureﾔ to prevent recurrence or, in advanced cancer, to keep it from growing and spreading.

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8
Q

Myelosuppressant

A

A chemotherapeutic agent that affects bone marrow and inhibits the formation of mature blood cells, particularly white blood cells, red blood cells and platelets.

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9
Q

Vesicant

A

A chemotherapeutic agent that causes redness and blistering on the skin. If such an agent is extravasated during intravenous administration, there will be severe damage to the tissue in the extravasation area.

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10
Q

Growth Fraction

A

The fraction of tumor cells that are in the replicative cycle (i.e., growth fraction)&raquo_space; influences their susceptibility to most chemotherapeutic agents.

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11
Q

High growth fraction vs. Low growth fraction

A

Cells that are rapidly dividing have a high growth fraction and are typically more susceptible to chemo than cells with a low growth fraction.

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12
Q

Cell-cycle specific

A

Chemotherapeutic agents that are only effective against high growth fraction cells

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13
Q

Cell-cycle nonspecific

A

effective against both high and low growth fraction cancers.

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14
Q

Significance of 1-g Tumor Mass

A

A total of 10^9 cells is the smallest tumor burden that is physically detectable; these 1 billion cells represent a tumor weighing about 1 g or about the size of a small grape; clinical symptoms usually first appear at this stage

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15
Q

Palliative Chemotherapy

A

Initial remissions are transient, with symptoms recurring between txs. Survival is extended, but the patient eventually dies of the disease.

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16
Q

Curative Chemotherapy (for disseminated cancers, such as leukemia)

A

Combination-drug chemo reduces the chance of drug resistance. Each drug chosen to have different cellular site of action or different cell-cycle specificity. Each drug chosen to have different organ toxicity.

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17
Q

Curative Chemotherapy (for solid cancers, such as testicular carcinoma)

A

Tumor burden is initially reduced by surgery and/or radiation; tx of occult micrometastases is continued after clinical signs of cancer have disappeared.

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18
Q

Susceptibility of cells to chemo

A

rapidly dividing have a high growth fraction and are typically more susceptible to chemo than cells with a low growth fraction. Also applies to normal cells that rapidly proliferate.

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19
Q

Normal cells most affected by chemo

A

1) Buccal mucosa
2) Upper GI tract (mouth, throat and esophagus)
3) Hair follicles
4) Bone marrow
5) Small intestine
6) Treatment-induced cancermo agents cause cancer years later.
7) Extravasation

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20
Q

Effects of chemo on buccal mucosa

A

stomatitis.

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21
Q

Effects of chemo on upper GI

A

mucositis.

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22
Q

Effects of chemo on hair follicles

A

hair loss or alopecia.

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23
Q

Effects of chemo on bone marrow

A

myelosuppression that can affect white blood cells (neutropenia), red blood cells (anemia) and platelets (thrombocytopenia).

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24
Q

Effects of chemo on small intestine

A

Interacts with the chemoreceptor trigger zone in the brain to cause nausea and vomiting.

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25
Q

Treatment-induced cancer

A

mutagenic effects of some chemo agents can cause cancer years later.

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26
Q

Extravasation

A

parenteral vesicants can cause significant soft tissue damage.

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27
Q

What are chemotherapy adjuncts (general)?

A

Treatments that help alleviate chemotherapy-induced side effects.

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28
Q

Why are chemotherapy adjuncts used?

A

1) THEY HELP ALLEVIATE CHEMOTHERAPY-INDUCED SIDE EFFECTS.
2) They help make the action of chemotherapy drugs
more effective.
3) They help alleviate symptoms of the cancer.

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29
Q

Chemotherapy adjuncts for stomatitis & mucositis

A

various medications alone or in compounded ‘magic mouthwash’ combinations

30
Q

Chemotherapy adjunct for alopecia

A

Cryotherapy (cold caps)

31
Q

Chemotherapy adjunct for myelosuppression

A

medications that stimulate the production of blood components

32
Q

Chemotherapy adjunct for chemo-induced N/V

A

medications are administered before and after chemo. Some act by affecting the chemoreceptor trigger zone

33
Q

Chemotherapy adjunct for chemo-induced N/V - drug classes

A

1) 5-HT3 receptor antagonists ﾖ dolasetron, granisetron, ondansetron and palonosetron.
2) Neurokinin-1 receptor antagonists ﾖ aprepitant and fosaprepitant.
3) Corticosteroid ﾖ dexamethasone (typically used in combination with a 5-HT3 receptor antagonist.
4) Other meds used in combination with some of the above include dronabinol (marijuana) and prochlorperazine.

34
Q

Combination vs. single agent chemo

A

Treating cancer with a combination of chemo agents is typically more effective than using a single agent.

35
Q

Using chemoagents with different toxicities/mechanisms

A

Can often be combined at full doses and result in higher response rates due to additive and/or potentiated cytotoxic effects and nonoverlapping toxicity to the patient.

36
Q

Using chemoagents with similar toxicities

A

Can only be combined safely by reducing the doses of each.

37
Q

Advantages of combination chemo

A
  1. Maximal cancer cell killing within the range of tolerated toxicity.
  2. A broader range of cancer cell lines in the heterogenous tumor population can be killed.
  3. The development of resistant cell lines may be delayed of prevented.
38
Q

Applicability of Combination protocols/regimens

A

applicable to one or more specific types of cancer.

39
Q

Typical Chemo Intervals

A

typically scheduled at intervals of about 21 days (intermittent therapy).

40
Q

Why use intervals in chemo?

A

allow for the patientﾒs immune system to recover from the chemo and reduce the risk of infection

41
Q

Antimetabolites

A

structurally similar to purine and pyrimidine bases and interfere with their availability by inhibiting their synthesis or competing with them in DNA and RNA synthesis. Most of the chemotherapeutic antimetabolites are either a purine or a pyrimidine analog.

42
Q

Common Adverse Effects of Cancer Chemotherapeutic Agents

A

1) Buccal mucosa ﾖ stomatitis.
2) Upper GI tract (mouth, throat and esophagus) ﾖ mucositis.
3) Hair follicles ﾖ hair loss.
4) Bone marrow ﾖ myelosuppression that can affect white blood cells (neutropenia), red blood cells (anemia) and platelets (thrombocytopenia).
5) Small intestine (with the chemoreceptor trigger zone in the brain) ﾖ nausea and vomiting.

43
Q

Origin of Chemotherapeutic antibiotics

A

isolated from different strains of Streptomyces fungus.

44
Q

General Actions of Chemotherapeutic Antibiotics

A

primarily act by interacting directly with DNA and disrupting its functions

45
Q

3 Specific Actions of Chemotherapeutic Antibiotics

A

1) interfering with RNA enzyme functions;
2) intercalating between DNA base pairs;
3) producing superoxide free radicals that cause DNA strands to break.

46
Q

Adverse Effects: Anthracyclines

A

THE ANTHRACYCLINES CAN CAUSE IRREVERSIBLE, DOSE-DEPENDENT CARDIOTOXICITY. This is due to the effects of superoxide radicals on the myocardium. The anthracyclines also causes the usual AEs and are vesicants.

47
Q

Uses: Bleomycin

A

treatment of testicular cancer, squamous cell carcinomas and some lymphomas

48
Q

Adverse Effects: Bleomycin

A

BLEOMYCIN CAN CAUSE PULMONARY TOXICITY that progresses from rales, cough and infiltration to potentially fatal PULMONARY FIBROSIS. The condition is sometimes referred to as bleomycin lung. The agent can also causes most of the common AEs with the unusual exception that myelosuppression is rare with bleomycin.

49
Q

MoA of Chemotherapeutic Antibiotics

A

1) Changes in a transport system can rapidly move the agent out of the cell following successful entry (e.g., P-glycoprotein).
2) Intracellular repair of DNA strand breaks by PARP enzymes.

50
Q

Alkylating Agents

A

cause the alkylation (i.e., the addition of an alkyl group) to the 7-nitrogen position on guanine in DNA.

51
Q

General Action: Alkylating Agents

A

Alkylation causes DNA strand fragmentation, interference with DNA replication and impaired protein synthesis.

52
Q

Adverse Effects: ALKYLATING AGENTS - Cyclophosphamide & Ifosfamide

A

Unique toxicity with both agents is due to the acrolein and other metabolites that are formed along with the active metabolite phosphoramide. These toxic metabolites can cause HEMORRHAGIC CYSTITIS AND FIBROSIS IN THE BLADDER. Adequate hydration and the drug MESNA help lessen those effects in the bladder.

53
Q

platinum complexes

A

carboplatin, cisplatin, & oxaliplatin

54
Q

platinum complexes MoA

A

Chemical structures include platinum. The mechanism of action is similar to that of the alkylating agents and involves the formation of inter- and intra- strand cross-links

55
Q

Adverse Effects: platinum complexes

A

All 3 agents cause the common AEs. Aggressive hydration is required with cisplatin to help prevent NEPHROTOXICITY.

56
Q

Effects of Interferons

A

Though the exact mechanism for the reaction is not known, the effects include suppression of cell proliferation, activation of macrophages and increased cytotoxicity of lymphocytes.

57
Q

Interferons

A

bind to cell surface receptors and this causes a series of complex intracellular reactions to take place. EFFECTS INCLUDE SUPPRESSION OF CELL PROLIFERATION, ACTIVATION OF MACROPHAGES, AND INCREASED CYTOXICITY OF LYMPHOCYTES

58
Q

Effects of Microtubule Inhibitors

A

affect the normal formation and function of the MITOTIC SPINDLE that is involved in METAPHASE, leading to cell death.

59
Q

Actions of Microtubule Inhibitors

A

1) formation of a dysfunctional spindle that cannot segregate the chromosomes during metaphase;
2) formation of overly stable microtubules that are nonfunctional during metaphase.

60
Q

Adverse Effects: Microtubule inhibitor - Vincristine

A

NEUROTOXICITY - Peripheral neuropathy, paresthesias and neuropathic pain.

61
Q

Tumors that are steroid hormone-sensitive may be either:

A

1) hormone responsive; 2) hormone dependent; or 3) both.

62
Q

Hormone Responsive Tumors

A

tumor regresses after treatment with a specific hormone

63
Q

Hormone Dependent Tumors

A

removal of a specific hormone causes tumor regression

64
Q

Aromatase

A

enzyme that catalyzes the conversion of testosterone and androstenedione to the estrogens estrone and estradiol

65
Q

Aromatase Inhibitors

A

DECREASE THE PRODUCTION OF ESTROGEN by blocking the activity of aromatase. This helps slow or stop the growth of hormone dependent tumors such as breast cancer.

66
Q

GnRH Analogs

A

goserelin and leuprolide

67
Q

Actions: Steroid hormones - GnRH (LHRH) analogs

A

Occupy the GnRH receptors in the pituitary. After an initial increase in LH and FSH secretion, the RECEPTORS ARE DESENSITIZED and the production of LH and FSH is inhibited. This results in DECREASED PRODUCTION OF ESTROGEN AND TESTOSTERONE

68
Q

Actions: Antiandrogens

A

directly compete with testosterone for binding on hormone dependent androgen receptors located on the prostate gland.

69
Q

Monoclonal antibody Production

A

produced using BIOTECHNOLOGY and are designed to INTERACT WITH SPECIFIC TARGETS in or on cancer cells and CAUSE CELLS TO STOP growing or to DIE.

70
Q

Actions: Monoclonal antibodies

A

1) BINDING to certain cancer cell PROTEINS or surface antigens and RECRUITING CYTOTOXIC IMMUNE SYSTEM mediators to ATTACK AND KILL the cancer cells;
2) binding to certain GROWTH FACTOR RECEPTORS on the of CANCER CELLS’ SURFACE, thereby INHIBITING the cell GROWTH PROCESSES, causing cell death;
3) binding to and INHIBITING cancer cell VASCULAR ENDOTHELIAL GROWTH FACTOR, thereby PREVENTING ANGIOGENESIS necessary for the cancer cells to grow.

71
Q

General Actions of Topoisomerase inhibitors

A

act on the essential DNA topoisomerase enzymes and cause effects that either STOP DNA REPLICATION or cause cancer cells to undergo APOPTOSIS.

72
Q

Specific Actions of Topisomerase Inhibitors

A

1) binding to topoisomerase-DNA complexes at sites of separation and PREVENT THE REJOINING OF STRANDS; 2) binding to DNA break sites and RENDER DNA strands SUSCEPTIBLE TO IRREVERSIBLE BREAKS.

Pharmacology (12 decks)

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