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CMOD Exam 2 > Cancer Chemotherapy Drugs > Flashcards

Cancer Chemotherapy Drugs Flashcards

(97 cards)

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1
Q

What are CCS drugs?

A

Cell Cycle Specific Drugs that are particularly effective during a specific phase of the cell cycle (Go).

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2
Q

What are CCNS drugs?

A

Cell Cycle Non-Specific Drugs that kill tumor cells in both cycling and resting phases of the cell cycle.

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3
Q

Growth Fraction

A

The proportion of cells in a tumor population that are actively dividing.

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4
Q

Log-Kill Hypothesis

A

A hypothesis meaning that anticancer drugs kill a fixed proportion of a tumor cell population, not a fixed number of tumor cells. i.e. 3-log-kill will reduce a populationfrom 10^6 to 10^3.

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5
Q

Myelosurpressant

A

A drug that surpresses the formation of mature blood cells such as erythrocytes, leukocytes, and platelets. This is known as “bone marrow surpression”

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6
Q

Oncogene

A

A mutant form of a normal gene that is found in naturally occurring tumors and which, when expressed in noncancerous cells, causes them to behave like cancer cells.

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7
Q

Rescue Therapy

A

The administration of endogenous metabolites to counteract the effects of anticancer drugs on normal (nonneoplastic) cells.

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8
Q

Vesicant

A

A drug that causes blisters on contact with tissues. Can be particularly damaging to veins if administered in high concentrations into small vessels.
i.e. Mechlorethamine

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9
Q

What phase of the cell cycle do the Vinca Alkaloids act on?

A

M

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10
Q

What phase of the cell cycle do the antimetabolites act on?

A

S (DNA Synthesis)

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11
Q

What phase of the cell cycle do the podophyllotoxins act on?

A

S (DNA Synthesis) and G2 (Synthesis of components needed for DNA Synthesis)

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12
Q

What phase of the cell cycle does Bleomycin act on?

A

G2 (Synthesis of components needed for DNA Synthesis)

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13
Q

What are the 6 methods of resistance to anticancer drugs?

A
  1. Increased DNA Repair
  2. Formation of Trapping Agents
  3. Changes in Target Enzymes
  4. Decreased Activation of ProDrugs
  5. Inactivation of Anticancer Drugs
  6. Decreased Drug Accumulaiton
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14
Q

Explain resistance via increased DNA repair and give examples of drugs that use this method.

A

The rate of repair of DNA damage is increased.

i.e. Alkylating Agents and Cisplatin

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15
Q

Explain resistance via formation of trapping agents and give examples of drugs that use this method.

A

Some tumor cells increase the production of thiol trapping agents (ex. glutathione) which interact with anticancer drugs that form reactive electrophilic species.
i.e. Bleomycin, Cisplatin, Anthracyclines

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16
Q

Explain resistance via changes in target enzymes and give examples of drugs that use this method.

A

Changes in the drug sensitivity of a target enzyme (ex. dihydrofolate reductase), and increased synthesis of the enzyme.
i.e. Methotrexate

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17
Q

Explain resistance via decreased activation of prodrugs and give examples of drugs that use this method.

A

Decrease in the activity of tumor cell enzymes needed to convert these prodrugs to their cytotoxic metabolites.
i.e. Purine Antimetabolites (Mercaptopurine and Thioguanine) and Pyrimidine Antimetaboites (Cytarabine and Fluorouracil)

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18
Q

Explain resistance via inactivation of anticancer drugs and give examples of drugs that use this method.

A

Increased activity of enzymes capable of inactivating anticancer drugs.
i.e. Most purine and pyrimidine antimetabolites

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19
Q

Explain resistance via increased decreased drug accumulation and give examples of drugs that use this method.

A

Increased expression of MDR1 gene for a cell surface glycoprotein (p-glycoprotein), which is the transport molecule involved in the accelerated efflux of many anticancer drugs in resistant cells.

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20
Q

Alkylating Agents

A

CCNS Drugs that form reactive molecular species that alkylate nucleophillic groups on DNA bases, especially the N-7 position on guanine. This leads to crosslinking of bases, abnormal base pairs, DNA strand breakage.

  1. Nitrogen Mustards (chlorampbucil, cyclophosphamide, meclorethamine)
  2. Nitrosoureas (carmustine, lomustine)
  3. Alkylsulfonates (busulfan)
  4. Cisplatin, Dicarbazine, Procarbazine
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21
Q

Describe the pharmacokinetics of CYCLOPHOSPHAMIDE:

A
  • CYP450 mediated biotransformation is needed for antitumor activity
  • Acrolein is a breakdown product
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22
Q

Describe the clinical uses of CYCLOPHOSPHAMIDE:

A
  1. Non-Hodgkins Lymphoma
  2. Breast and Ovarian Cancers
  3. Neuroblastoma
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23
Q

Describe the toxicity of CYCLOPHOSPHAMIDE:

A
  1. GI Distress
  2. Myelosurpression
  3. Alopecia
  4. Hemorrhagic Cystitis (from formation of acrolein; reduced by vigorous hydration and mesna)
  5. Cardiac Dysfunction
  6. Pulmonary Toxicity
  7. Inappropriate ADH secretion
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24
Q

Describe the mechanism and pharmacokinetics of MECLORETHAMINE.

A

Spontaneously converts in the body to a reactive cytotoxic product.

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25
Describe the clinical uses of MECLORETHAMINE.
Hodgkin's Lymphoma
26
Describe the toxicity of MECLORETHAMINE.
1. GI Dictress 2. Myelosurpression 3. Sterilization 4. Marked vesicant action
27
Describe the pharmacokinetics of the Platinum Analogues (CISPLATIN, CARBOPLATIN, OXALIPLATIN).
- Given IV - Distributes to most tissues. - Cleared unchanged from the kidneys
28
Describe the clinical uses of the Platinum Analogues (CISPLATIN, CARBOPLATIN, OXALIPLATIN).
Cisplatin amd Carboplatin 1. Testicular Carcinoma 2. Bladder, Lung, and Ovarian Cancer Oxaliplatin 1. Advanced colon cancers
29
Describe the toxicity of the Platinum Analogues (CISPLATIN, CARBOPLATIN, OXALIPLATIN).
1. GI Distress 2. Mild Hematotoxicity 3. Neurotoxic (peripheral neuritis & acoustic nerve damage) 4. Nephrotoxic (**may be reduced by the use of mannitol with forced hydration)
30
Compare the toxicities of Carboplatin and Cisplatin.
Carboplatin is less nephrotoxic and less likely to cause tinnitus and hearing loss but has greater myelosurpressive actions.
31
What is different about the toxicity of Oxaliplatin from the other platinum analogues?
It causes dose-limited neurotoxicity.
32
Describe the mechanisms of PROCARBAZINE.
It is a reactive agent that forms hydrogen peroxide, which generates free radicals that cause DNA strand scission.
33
Describe the pharmacokinetics of PROCARBAZINE.
- Orally active - Penetrates most tissues including CSF - Eliminated via hepatic metabolism
34
Describe the clinical uses of PROCARBAZINE.
Hodgkin's Lymphoma
35
Describe the toxicity of PROCARBAZINE.
1. Myelosurpression 2. GI Irritation 3. CNS Dysfunction 4. Peripheral Neuropathy 5. Skin Reactions 6. Inhibits many enzymes (i.e. MAO and enzymes involved in hepatic elimination) 7. Leukemogenic * *Disulfram-like reactions have occurred with EtOH use.
36
Busulfan
- used to treat chronic myelogenous leukemia | - causes adrenal insufficiency, pulmonary fibrosis, and skin pigmentaiton
37
Carmustine (BCNU) and Lomustine (CCNU)
highly lipid soluble drugs that are used as adjuncts in the management of brain tumors
38
Dicarbazine
- used for Hodgkin's Lymphoma | - causes alopecia, skin rash, GI distress, myelosurpression, phototoxicity, and flu-like syndrome
39
Antimetabolites
CCS drugs that are structurally similar to and are antagonists of endogenous compounds and act primarily on the S phase of the cell cycle. 1. Folic Acid Antagonists (Methotrexate) 2. Purine Antagonists (Mercaptopurine, Thioguanine) 3. Pyrimidine Antagonists (Flurouraacil, Cytarabine, Gemcitabine)
40
Describe the mechanisms of action of METHOTREXATE.
- Substrate for and inhibitor of dihydrofolate reductase. (DHFR). - Leads to a decrease in the synthesis of thimidylate, purine nucleotides, and amino acids. Therefore, interfering with nucleic acid and protein metabolism. * **Formation of Polyglutamate derivatives is important for its cytotoxic actions
41
Describe the mechanisms of resistance of METHOTREXATE.
1. Decreased drug accumulation. 2. Changes in drug sensitivity or activity of DHFR 3. Decreased formation of polyglutamates.
42
Describe the pharmacokinetics of METHOTREXATE.
- Oral and IV administration - Good tissue distribution except for CNS - Not metabolized - Renal clearance * *Adequate hydration is needed to prevent crystallization in renal tubules
43
Describe the clinical uses of METHOTREXATE.
1. Choriocarcinoma 2. Acute Leuken=mias 3. Non-Hodgkin's and cutaneous T-cell Lymphomas 4. Breast Cancer 5. Rheumatoid Arthritis Psoriasis 6. Ectopic Pregnancy and Abortion
44
Describe the toxicity of METHOTREXATE.
1. Bone Marrow surpression 2. GI Distress 3. Toxic effects on skin 4. Hepatotoxicity (long term use) 5. Pulmonary Infiltrates and Fibrosis (long term)
45
Leucovorin Rescue
Reduction of the toxic effects of methotrexate on normal cells by the administration of folinic acid (leucovorin)
46
What drugs enhance the toxicity of Methotrexate?
NSAIDs, Salicylates, sulfonamides, sulfonylureas
47
Describe the mechanism of action of MERCAPTOPURINE (6-MP) and THIOGUANINE (6-TG).
Both are purine antimetabolites that are activated by hypoxanthine-guaninephosphoribisyltransferases (HGPRTases) to toxic nucleotides that inhibit several enzymes involved in purine metabolism.
48
Describe the mechanism of resistance of MERCAPTOPURINE (6-MP) and THIOGUANINE (6-TG).
- Resistant tumor cells have decreased HGPRTase activity. | - They also increase their production of alkaline phosphatases that inactivate toxic nucleotides.
49
Describe the pharmacokinetics of MERCAPTOPURINE (6-MP) and THIOGUANINE (6-TG).
- Low oral bioavailability because of first pass hepatic metabolism. - Metabolism of 6-MP by xanthine oxidase is inhibited by allopurinol.
50
Describe the clinical uses of MERCAPTOPURINE (6-MP) and THIOGUANINE (6-TG).
1. Acute leukemias | 2. Acute Myelocytic Leukemia
51
Describe the toxicity of MERCAPTOPURINE (6-MP) and THIOGUANINE (6-TG).
- Bone marrow surpression is dose limiting. | - Hepatic dysfunction (cholestasis, jaundice, necrosis) also occurs.
52
Describe the mechanism of action of FLUOROURACIL (5-FU).
Converted in cells to 5-FdUMP which inhibits thymidylate synthase and leads to the "thymineless death" of cells.
53
Describe the mechanism of resistance of FLUOROURACIL (5-FU).
- Decreased activation of 5-FU - Increased Thymidylate Synthase activity - Reduced drug sensitivity of the enzyme.
54
Describe the pharmacokinetics of FLUOROURACIL (5-FU).
- Widely distributed when given IV (including CSF) | - Elimination os mainly by metabolism
55
Describe the clinical uses of FLUOROURACIL (5-FU).
- Bladder, breast, colon, head, neck, liver, and ovarian cancers - Used topically for keratosis and superficial basal cell carcinoma
56
Describe the toxicity of FLUOROURACIL (5-FU).
- Gi Dictress - Myelosurpression - Alopecia
57
Describe the mechanism of action of CYTARABINE (ARA-C).
Pyrimidine antimetabolite that is activated by kinases to AraCTP, an inhibitor of DNA polymerases. ***Most specific drug for S pahse of cell cycle
58
Describe the mechanism of resistance of CYTARABINE (ARA-C).
Occurs via decreased uptake or decreased conversion to AraCTP.
59
Describe the mechanisms of GEMCITABINE.
- It is a deoxycitadine analog that is converted into the active diphosphate and triphosphate nucleotide form. - Gemcitabine diphosphate inhibits ribonucleotide reductase and diminishes the supply of deoxyribonucleoside triphosphates required for DNA synthesis. - Gemcitabine triphosphate can be incorporated into DNA and cause chain termination.
60
Describe the pharmacokinetics of GEMCITABINE.
Elimination is mainly via metabolism.
61
Describe the clinical uses of GEMCITABINE.
1. Pancreatic Cancer 2. Non-small cell lung cancer 3. Bladder cancer 4. Non-Hodgkin's Lymphoma
62
Describe the toxicities of GEMCITABINE.
- Primarily myelosurpression via neutropenia. | - Pulmonary Toxicity has been observed.
63
Plant Alkaloids
CCS Drugs 1. Vinca Alkaloids (vinblastine, vincristine, vinorelbine) 2. Podophylotoxins (etoposide, teniposide) 3. Camptothecins (topotecan, irinotecan) 4. Taxanes (paclitaxel, docetaxel)
64
Describe the MOA of the Vinca Alkaloids (VINCRISTINE, VINBLASTINE, VINORELEBINE).
Block formation of the mitotic spindle by preventing the assembly of tubulin dimers into microtubules. Act primarily on the S phase.
65
Describe the mechanisms of resistance of the Vinca Alkaloids (VINCRISTINE, VINBLASTINE, VINORELEBINE).
Increased efflux of the drug form cells via the membrane drug transporter.
66
Describe the pharmacokinetics of the Vinca Alkaloids (VINCRISTINE, VINBLASTINE, VINORELEBINE).
- Must be given parentally. - Penetrate most tissues except CSF - Cleared mainly via biliary ecretion
67
Describe the clinical uses of the Vinca Alkaloids (VINCRISTINE, VINBLASTINE, VINORELEBINE).
- Vincristine: acute leukemias, lymphomas, Wilm's tumor, choriocarcinoma - Vinblastine: lymohomas, neiroblastomas, testicular carcinoma, Kaposi sarcoma - Vinorelbine: non-small cell lung cancer and breast cancer
68
Describe the toxicities of the Vinca Alkaloids (VINCRISTINE, VINBLASTINE, VINORELEBINE).
GI distress, alopecia, bone marrow surpression. **Vincristine does not cause serious myelosurpression but has neurotoxic actions such as areflexia, peripheral neuritis, paralytic ileus
69
Describe the mechanisms of the Podophylotoxins (ETOPOSIDE and Teniposide).
Increase degradation of DNA via an interaction with topoisomerase II and also inhibits the ETC. **Most active during late S and early G2 phase.
70
Describe the pharmacokinetics of the Podophylotoxins (ETOPOSIDE and Teniposide).
- Well absorbed orally - Distributes to most tissues - Mainly renal elimination * *Dose reductions should be made in patients with renal impairment.
71
Describe the clinical uses of the Podophylotoxins (ETOPOSIDE and Teniposide).
Used in combination drug therapy for lung (small cell), prostate and testicular carcinoma.
72
Describe the toxicites of the Podophylotoxins (ETOPOSIDE and Teniposide).
GI Irritants Alopecia Bone Marrow Suppression
73
Describe the mechanisms of the Camptothecins (TOPOTECAN and IRINOTECAN).
Inhibit topoisomerase I. They damage DNA by inhibiting the enzyme that cuts and regulates single DNA strands during normal DNA repair processes.
74
Describe the pharmacokinetics of the Camptothecins (TOPOTECAN and IRINOTECAN).
Irinotecan: a prodrug that is converted in the liver into an active metabolite and is eliminated in the bile and feces Topotecan: eliminated renally
75
Describe the clinical uses of the Camptothecins (TOPOTECAN and IRINOTECAN).
Topotecan: second line therapy for advanced ovarian cancer and for small cell lung cancer. Irinotecan: used for metastatic colon cancer
76
Describe the toxicities of the Camptothecins (TOPOTECAN and IRINOTECAN).
Myelosurpression and diarrhea.
77
Describe the mechanisms of the Taxanes (PACLITAXEL and DOCETAXEL).
Interfere with the mitotic spindle by preventing microtubule disassembly into tubulin monomers.
78
Describe the pharmacokinectics of the Taxanes (PACLITAXEL and DOCETAXEL).
Given IV
79
Describe the clinical uses of the Taxanes (PACLITAXEL and DOCETAXEL).
Advanced breast and ovarian cancers
80
Describe the toxicities of the Taxanes (PACLITAXEL and DOCETAXEL).
Paclitaxel: neutropenia, thrombocytopenia, peripheral neuropathy, hypersensitivity reactions during infusion. Docetaxel: neurotoxicity and bone marrow surpression.
81
Antibiotics in Chemotherapy
Several structurally dissimilar agents that act as antineoplastic drugs.
82
Describe the mechanisms of DOXORUBICIN and DAUNORUBICIN. (Anthracyclines)
- CCNS drugs - Intercalate between base pairs, inhibit topoisomerase II, and generate free radicals. - Block the synthesis of DNA, RNA, and cause DNA strand scission. - This causes membrane disruption to occur.
83
Describe the pharmacokinetics of DOXORUBICIN and DAUNORUBICIN.
- Given IV - Metabolized in the liver - Products are excreted in the bile and urine.
84
Describe the clinical uses of DOXORUBICIN and DAUNORUBICIN.
Doxorubicin: Hodgkin's Lymphoma, myelomas, sarcomas, breast, endometrial, lung, ovarian, and thyroid cancer. Daunorubcin: acute leukemias Idarubicin: acute myelogenous leukemias
85
Describe the toxicities of DOXORUBICIN and DAUNORUBICIN.
- Bone marrow surpression, GI distress, severe alopecia. - Cardiotoxicity (ECG abnormalities, cardiomyopathy and CHF). * **Dexrazoxane (inhibitor of iron mediated free radical generation) may protect against cardiotoxicity. * **Liposomal formulaitons of doxorubicin may be less cardiotoxic.
86
Describe the mechanisms of Bleomycin.
Mixture of glycopeptides that generates free radicals that bind to DNA, cause strand breaks, and inhibit DNA synthesis. **CCS drug active during G2.
87
Describe the pharmacodynamics of Bleomycin.
- Given parentally - Inactivated by tissue aminopeptidases - Some renal clearance of intact drug also occurs.
88
Describe the clinical uses of Bleomycin.
Hodgkin's lymphoma, testicular cancer, lymphomas, squamous cell carcinomas
89
Describe the toxicities of Bleomycin.
- Pulmonary dysfunction which develops slowly and is dose limiting. - Hypersensitivity reactions - Mucocutaneous reactions (alopecia, blister formation, hyperkeratosis)
90
Describe the mechanism of Dactinomycin.
CCNS drug that that binds to dsDNA and inhibits DNA dependent RNA synthesis.
91
Describe the pharmacokinetics of Dactinomycin.
- Given parentally. | - Both intact drug and metabolites are excreted in the bile.
92
Describe the clinical uses of Dactinomycin.
Melanoma and Wilm's Tumor
93
Describe the toxicities of Dactinomycin.
Bone marrow suppression, skin reactions, GI irritation.
94
Describe the mechanism of Mitomycin.
CCNS drug that is metabolized by the liver to form an alkylating agent that crosslinks DNA.
95
Describe the pharmocokinectics of Mitomycin.
Given IV and is rapidly cleared via hepatic metabolism.
96
Describe the clinical uses of Mitomycin.
- Acts against hypoxic tumor cells. | - Used in combo regimens for adenocarcinomas of the cervix, stomach, pancreas, and lung.
97
Describe the toxicities of Mitomycin.
- Severe myelosurpression | - Toxic to heart , lung, liver, kidney

CMOD Exam 2 (7 decks)

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