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Pharmacology II > Exam 3: Antineoplastic agents > Flashcards

Exam 3: Antineoplastic agents Flashcards

1
Q

Define Cancer:

A

A disease of cell proliferation where normal cells are transformed by genetic mutation into cells with dysregulated growth.

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2
Q

What are the 3 steps of Carcinogenesis:

A
  1. Transformation
  2. Proliferation
  3. Metastasis
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3
Q

Define the transformation step of carcinogenesis:

A
  • A cell with normal growth changes into a cell with dysregulated growth (Malignancy)
  • Genetic Damage
    ○ Inherited
    ○ Mutations that alter growth and repair
    ○ Alterations in or loss of regulatory proteins
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4
Q

Define the Proliferation phase of Carcinogenesis

A
  • Growth of transformed cells into a tumor

- Increase in the number of cells

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5
Q

Most antineoplastic drugs target what activity?

A

Target dividing cells

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6
Q

Which cells respond best to chemotherapy?

A
  • Small, rapidly dividing cells respond best

- Normal cells also rapidly divided and are also subjected to effects of chemo

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7
Q

Define Dose-limiting toxicity

A

The dosage being administered is limited because of the possibility of causing toxicity

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8
Q

What is the challenge of chemotherapy?

A

To give an adequate dose to kill the cancer cells without killing too many healthy cells

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9
Q

Define the Metastasis phase of Carcinogenesis

A
  • Cancer cells acquire the ability to invade tissues throughout the body
  • Tumor cells mutate which allows them to invade into tissues and vessels, body cavities, etc. and grow in a new location.
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10
Q

What must be taken into consideration before administering chemotherapy to a patient with metastatic lesions?

A
  • As these cells gain mutations, their response to chemotherapy may change. (altered receptors)
  • The original tumor may respond well to chemotherapy, but metastatic lesions may be less response = poor prognosis
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11
Q

Most chemotherapy agents interfere with what carcinogenesis phase?

A

Cell proliferation

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12
Q

When are cancer cells most sensitive to chemotherapy drugs?

A
  • When the cells are actively going through the cell cycle

- Metabolically active cells are more susceptible to drugs that interfere with cell growth and division

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13
Q

What is the tumor suppressor gene that senses DNA damage and arrests the cell cycle?

A
  • p53

This allows time for the damage to be repaired

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14
Q

If a cell fails to repair damage due to chemotherapy, what occurs?

A
  • The cell dies by a biochemically-driven programmed cell death
  • *apoptosis
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15
Q

What is the action of p53?

A
  • Helps to suppress cancer; anti-cancer mechanisms.
  • Activate DNA repair proteins
  • Hold cell cycle at G1/S regulation point so that DNA repair proteins will fix damage, then cell allowed to continue cell cycle.
  • Can initiate apoptosis if damage is irreparable
  • Induce growth arrest.
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16
Q

What things might induce p53?

A
  1. UV radiation
  2. Oncogenes
  3. DNA damaging drugs
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17
Q

What occurs if p53 gene is damaged?

A

Tumor suppression is severely reduced.

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18
Q

Which type of cells are “highly responsive to chemotherapy”?

A
  • Cancer cells that express p53

* includes leukemias, lymphomas, testicular cancer

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19
Q

Which cells are minimally responsive or resistant to DNA-damaging chemotherapy drugs?

A
  • Cancer cells that acquire a mutation in p53

* include pancreatic, lung and liver cancers

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20
Q

T or F, Every malignant cell MUST be destroyed to “cure” the cancer

A

True, a single malignant cell can expand clonally to give rise to a tumor.

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21
Q

When administering chemotherapy, is there a specific dosage or cycle number that all therapies follow?

A

Multiple cycles of chemotherapy must be given at the HIGHEST tolerable dose with the most frequent tolerable interval to achieve a cure

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22
Q

Chemotherapy is under what order of kinetics?

A
  • First-order kinetics

A constant fraction of tumor cells is killed with each cycle of chemotherapy

23
Q

Which type of tumors do not respond well to chemotherapy?

A
  • Solid tumors

Slower growth/division of these cells

24
Q

Solid tumors often require what type of treatment?

A

Often require radiation and/or surgery as well as chemotherapy.

  • Resistance to chemotherapy drugs often develops!
    - Justification for using combination drug therapy
25
Q

Explain Combination Chemotherapy

A

(B) Includes drugs that act on different molecular targets, at different phases of the cell cycle and with different dose-limiting toxicities.

26
Q

Explain the benefits to Combination Chemotherapy

A
  • This reduces the emergence of drug resistance
  • Allows each individual drug to be given at its highest tolerable dose.
  • (B) Some regimens offer SYNGERGISTIC BENEFITS
  • (B) Typically use intermittent dosing
27
Q

Examples of cancers that require combination chemotherapy

A
  • Hodgkin’s disease
  • Testicular cancer
  • Breast cancer
  • Ovarian cancer
  • Cervical cancer
  • Bladder cancer
  • Lung cancer
  • Cancer of head and neck
28
Q

The current emphasis in cancer treatment is use of what therapy? Why?

A
  • Drug Combination therapy
  • It takes into account phase of the cell cycle
  • Potential synergistic action
  • Increases efficacy
  • Decreases cell resistance
29
Q

Define Cell-Cycle specific drugs

A

Drugs that affects one phase

30
Q

Define Cell-Cycle non-specific drugs

A

Drug affects any/all phases

31
Q

T or F, Drugs for chemotherapy are safe for humans to consume (B)

A
  • False, they are not safe.

(B) They lack specificity. They affect malignant cells as well as rapid but normally proliferating cells

32
Q

Name some examples of normal proliferating cells that chemotherapy drugs also attack

A

Bone marrow, Skin & intestinal mucosa

33
Q

(B)What are the signs of toxicity that appear in the normal cell proliferating areas that are attacked by chemo drugs

A
  • Blood dyscrasias
  • Ulcerations of oral mucosa and other sites in GI tract
  • Nausea/vomiting
34
Q

(B)Mechanism of Alkylating agents

A
  • (B)Transfer alkyl groups to important cell constituents with amino-, sulfhydryl-, carboxyl-, and phosphate- groups
  • (B)Alkylate DNA, probably at guanine as the primary mechanism for cell death
  • (B)Interfere with DNA, RNA and proteins to prevent cell metabolism and division
35
Q

What is the primary mechanism for cell death

A

Alkylate DNA, probably at guanine

36
Q

Name the major classes of Alkylating agents

A
  1. Nitrogen mustards
  2. Alkyl sulfonates
  3. Ethylenimines
  4. Triazines
  5. Nitrosureas
37
Q

T or F, Susceptibility to infection is common outcome of treatment with alkylating agents

A
  • True

They are mutagenic, teratogenic, oncolytic, myelosuppressive, immunosuppressive and carcinogenic.

38
Q

Name the 3 given examples of Alkylating agents

A
  1. Cyclophosphamide (Cytoxan)
    a. Multiple cancers, bone marrow transplants
  2. Ifosfamide (Ifex) = nitrogen mustard
    a. Multiple cancers
  3. Procarbazine (Matulane)
    a. Hodgkin’s disease
39
Q

Role of Antimetabolites

A
  • Serve as fraudulent substrates for biochemical interactions
  • Interfere with growth of rapidly proliferating cells
40
Q

Are Antimetabolites cycle specific or non-specific?

A
  • Specific

- (B) S phase specific

41
Q

Name the classes of Antimetabolites

A
  • Folic acid antagonists
  • Purine antagonists
  • Pyrimidine antagonists
42
Q

Action of Folic acid antagonists

A
  1. (B) Inhibits DNA synthesis

2. Inhibit nucleic acid synthesis by blocking the enzyme dihydrofolate reductase

43
Q

Name the Folic acid antagonist drug

A
  • (B) Methotrexate (Rheumatrex, Trexall)

- Used for many cancers; autoimmune diseases

44
Q

Is methotrexate cell cycle specific or non-specific?

A
  • (B) Cell-cycle specific

* *S phase

45
Q

Role of Purine antagonists

A

Inhibit enzymes that convert hypoxanthine ribonucleotide to adenine and xanthine ribonucleotide

46
Q

Name the purine antagonist drug name

A
  • (B) Mercaptopurine (purinethol)

- Lymphoblastic leukemia

47
Q

Function of mercaptopurine

A

Inhibits DNA and RNA synthesis

48
Q

Is mercaptopurine cell-cycle specific or non-specific

A
  • (B) Cell-cycle specific

* *S phase

49
Q

Role of Pyrimidine antagonists

A

Inhibit pyrimidine synthesis

50
Q

Name the 2 drugs in the pyrimidine antagonist class

A
  1. (B) Fluorouracil (Adrucil) = “5-FU”

2. (B) Cytarabine (Cytosar-U) = “Ara-C”

51
Q

Function of fluorouracil

A
  • Interferes with DNA synthesis or becomes incorporated into RNA
  • Many cancers
52
Q

Function of cytarabine

A

Inhibition of DNA synthesis and repair

53
Q

Are Pyrimidine antagonists cell-cycle specific or non-specific?

A
  • (B) Specific

* *S phase

Pharmacology II (24 decks)

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