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OBGYN > Principles of Chemotherapy > Flashcards

Principles of Chemotherapy Flashcards

1
Q

Define growth fraction.

A

the proportion of cells in a tumor that are actively involved in cell division

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2
Q

How does growth fraction impact our management of tumors?

A
  • it is the proportion of cells in a tumor that are actively involved in cell division
  • the larger the tumor, the smaller the fraction due to vascular and oxygen constraints
  • therefore, tumor debunking increases the growth fraction, making the tumor more vulnerable to chemotherapy and radiation
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3
Q

Define generation time.

A

the length of the cell cycle, from one M phase to the next

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4
Q

For a given cell type, which phases of the cell cycle are constant and which vary?

A

S and M are relatively constant whereas G1 and G2 vary

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5
Q

Chemotherapy and radiation kill tumor cells by what order of kinetics and what does this mean?

A

first-order kinetics, meaning each dose kills a constant fraction of tumor cells rather than a constant number

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6
Q

Why do we use many small doses of chemotherapy or radiation rather than a large, 1 time dose?

A
  • several intermittent doses are more effective since these therapies work via first-order kinetics and kill a constant fraction rather than constant number of tumor cells
  • furthermore, this method reduces side effects
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7
Q

Which kinds of chemotherapeutic agents are more useful in tumors with a low growth fraction? Which are more useful in tumors with a high growth fraction?

A
  • those that are cell cycle nonspecific are effective in tumors with a low growth fraction
  • those that are cell cycle specific are effective in tumors with a larger growth fraction
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8
Q

Describe the mechanism of action and primary toxicities of alkylating agents. Give an example or two of specific drugs.

A
  • they bind and cross-link DNA inter strand, intrastrand, or to proteins, thus preventing replication and transcription
  • they are likely to cause hemorrhagic cystitis, alopecia, and nephrotoxicity
  • includes cyclophosphamide, ifosfamide, and melphalan
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9
Q

Describe the mechanism of action and primary toxicities of alkylating-like agents. Give an example or two of specific drugs.

A
  • they cross-link DNA strands in an interrstrand fashion
  • they are likely to cause nephrotoxicity, neurotoxicity, and myelosuppression
  • includes cisplatin, carboplatin, and doxorubicin
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10
Q

Describe the mechanism of action and primary toxicities of antibiotic chemotherapies. Give an example or two of specific drugs.

A
  • they interfere with DNA replication through free radical formation and intercalation between bases
  • they have varying toxicities
  • includes bleomycin and actinomycin D
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11
Q

Describe the mechanism of action and primary toxicities of antimetabolite chemotherapies. Give an example or two of specific drugs.

A
  • they block the enzymes required for DNA synthesis, thus they are most active in the S phase of the cell cycle
  • likely to cause GI, myelosuppression, dermatologic, and hepatotoxicities
  • includes MTX and 5-FU
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12
Q

Describe the mechanism of action and primary toxicities of mitotic inhibitors. Give an example or two of specific drugs.

A
  • work by inhibiting microtubule assembly
  • likely to cause myelosuppression
  • includes vincristine, vinblastine, and paclitaxel
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13
Q

Describe the mechanism of action and primary toxicities of topoisomerase inhibitors. Give an example or two of specific drugs.

A
  • inhibit topoisomerase, resulting in DNA strand breaks
  • likely to cause myelosuppression, alopecia, and GI side effects
  • includes etoposide and topotecan
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14
Q

Which blood cell types are most susceptible to the myelosuppressive effects of chemotherapy?

A
  • erythroid cells
  • neutrophils
  • megakaryocytes
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15
Q

What is the difference between a sequential chemotherapeutic blockade and a concurrent blockade?

A
  • sequential refers to the use of two or more drugs that block sequential enzymes in a single biochemical pathway
  • concurrent refers to the use of two or more drugs that attack parallel biochemical pathways leading to the same end product
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16
Q

What is adjuvant chemotherapy?

A

a course of combination chemotherapy that is given in a high dose to patients who have no evidence of residual cancer after radiotherapy or surgery with the purpose of eliminating any residual cancer cells

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17
Q

What is neoadjunvant chemotherapy?

A

a course of chemotherapy that aims to eradicate micro metastases or to reduce inoperable disease to prepare patients for surgery and/or radiotherapy

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18
Q

What is induction chemotherapy?

A

a combination chemotherapy given in a high dose to cause remission

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19
Q

What is maintenance chemotherapy?

A

a long-term, low-dose regimen given to a patient in remission to maintain the remission by inhibiting the growth of remaining cancer cells

20
Q

In brief what are adjuvant, neoadjuvant, induction, and maintenance chemotherapy?

A
  • adjuvant is given in high dose after radiation or surgery to eliminate residual cancer
  • neoadjuvant is given prior to radiation or surgery to eliminate micro metastases or reduce inoperable disease
  • induction is high dose chemo used to induce remission
  • maintenance is long-term, low-dose chemo used to maintain remission by inhibiting growth of residual cancer
21
Q

How do SERMs affect estrogen signaling?

A

SERMs bind estrogen receptors and allow them to bind to chromosomes but inhibits their ability to activate cell metabolism when they do

22
Q

What is anastrozole?

A

an aromatase inhibitor which suppresses intratumor and plasma estrogen levels

23
Q

What is letrozole?

A

an aromatase inhibitor which suppresses intratumor and plasma estrogen levels

24
Q

What is the major side effect of aromatase inhibitors?

A

they are associated with bone loss secondary to the induced hypoestrogenic state

25
Q

How does ionizing radiation treat cancer?

A

it causes the production of free hydrogen ions and hydroxyl radicals; with sufficient oxygen, hydrogen peroxide is formed and disrupts the structure of DNA

26
Q

What are the four “Rs” of radiation therapy?

A

four principles that account for the benefit of fractionated radiation doses compared to one large does

  • repair of sublethal injury: when a dose is divided, the number of normal cells that survive is greater and the dose is better tolerated
  • repopulation: reactivation of stem cells occurs when radiation is stopped, so regenerative capacity depends on the number of available stem cells
  • reoxygenation: cells are most vulnerable to radiation damage with oxygen present and divided doses allow tumor cells to be brought into contact with capillaries between doses
  • redistribution in the cell cycle: fractionated doses make it more likely that a given cell is irradiated when it is actively dividing
27
Q

What is teltherapy?

A

a form of radiation therapy, usually used to shrink the tumor before localized radiation, which depends on the use of high-energy beams to spare the skin and deliver less toxic radiation to the bone

28
Q

What is brachytherapy?

A

a form of radiation therapy that depends on the inverse square law stating that the dose of radiation at a given point is inversely proportion to the square of the distance from the radiation source; it uses encapsulated sources of ionizing radiation implanted directly into the tumor tissue

29
Q

What are the acute reactions of radiation therapy?

A
  • the most immediate complications, which involve rapidly dividing tissues
  • this includes the skin, GI mucosa, bone marrow, and reproductive cells
  • manifesting ase enteritis, acute cystitis, vulvititis, proctosigmviditis, topical skin desquamation, and bone marrow depression
30
Q

What are the chronic complications of radiation therapy?

A
  • those that occur months to years after completion of therapy
  • includes obliteration of small blood vessels or thickening of the vessel wall, fibrosis, and reductions in epithelial and parenchymal cell populations
  • manifesting as proctitis, hemorrhagic cystitis, formation of ureterovaginal and vesicovaginal fistulas, rectal or sigmoid stenosis, GI fistulas, and bowel obstructions
31
Q

What is trastuzumab?

A

a monoclonal antibody to the human epidermal growth factor receptor 2 protein (HER-2), which is sometimes over expressed by breast cancer or gynecologic cancers

32
Q

What is bevacizumab?

A

a monoclonal antibody against VEGF, which inhibits angiogenesis in tumors and is used in the treatment of cervical and epithelial ovarian cancer

33
Q

What is the mechanism of action and dose-limiting toxicity of paclitaxel?

A
  • it is a mitotic inhibitor

- use is limited by neutropenia and peripheral neuropathy

34
Q

What is the mechanism of action and dose-limiting toxicity of carboplatin?

A
  • it is an alkylating-like agent

- use is limited by thrombocytopenia

35
Q

What is the mechanism of action and dose-limiting toxicity of cisplatin?

A
  • it is an alkylating-like agent

- use is limited by nephrotoxicity

36
Q

What is the mechanism of action and dose-limiting toxicity of bleomycin?

A
  • it is a tumor antibiotic

- use is limited by pulmonary fibrosis

37
Q

What is the mechanism of action and dose-limiting toxicity of topotecan?

A
  • it is a topoisomerase inhibitor

- use is limited by neutropenia

38
Q

What is the mechanism of action and dose-limiting toxicity of liposomal doxorubicin?

A
  • it is an alkylating-like agent

- use is limited by myelosuppression and cardiac toxicity

39
Q

What is the mechanism of action and dose-limiting toxicity of gemcitabine?

A
  • it is an antimetabolite

- use is limited by neutropenia

40
Q

What is the mechanism of action and dose-limiting toxicity of etoposide?

A
  • it is an topoisomerase inhibitor

- use is limited by myelosuppression

41
Q

What is the mechanism of action and dose-limiting toxicity of ifosfamide?

A
  • it is an alkylating agent

- use is limited by hemorrhagic cystitis

42
Q

What is the mechanism of action and dose-limiting toxicity of methotrexate?

A
  • it is an antimetabolite

- use is limited by myelosuppression

43
Q

What is the mechanism of action and dose-limiting toxicity of actinomycin D?

A
  • it is a tumor antibiotic

- use is limited by myelosuppression

44
Q

What is the mechanism of action and dose-limiting toxicity of cyclophosphamide?

A
  • it is an alkylating agent

- use is limited by myelosuppression

45
Q

What is the mechanism of action and dose-limiting toxicity of vincristine?

A
  • it is a mitotic inhibitor

- use is limited by myelosuppression

OBGYN (21 decks)

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