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POD III > Cancer Chemotherapy > Flashcards

Cancer Chemotherapy Flashcards

1
Q

What 2 chemotherapy combinations are used to treat Hodgkin’s disease?

A
  1. MOPP

2. ABVD

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2
Q

What chemotherapy combination is used to treat Non-Hodgkin’s lymphoma?

A

CHOP

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3
Q

What chemotherapy combinations are used to treat breast cancer?

A
  1. CMF

2. CAF

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4
Q

What chemotherapy combination is used to treat small cell lung cancer?

A

PACE

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5
Q

What chemotherapy combination is used to treat germ cell?

A

VIP

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6
Q

What chemotherapy combination is used to treat cervical cancer?

A

BIP

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7
Q

What chemotherapy combination is used to treat lymphomas?

A

M-BACOD

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8
Q

What chemotherapy combination is used to treat ovarian cancer?

A

BEP

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9
Q

What chemotherapy combination is used to treat pheochromocytoma?

A

CVD

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10
Q

What chemotherapy combination is used to treat testicular cancer?

A

PEB

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11
Q

The up-regulation of p-glycoprotein pumps affects cancer drugs in what way?

A

Promotes the efflux of drugs out of the cell and therefore makes the cancer cell resistant to the action of the drugs.

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12
Q

What is cross linking DNA and what type of drugs use this mechanism?

A
  • Blocks DNA replication and transcription by linking two bases of DNA.
  • Alkylating agents
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13
Q

What alkylating agents are taken as prodrugs?

A

Cyclophosphamide and iphosphamide.

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14
Q

What cytotoxic agent is produced when cyclophosphamide and iphosphamide undergo oxidative phosphorylation?

A

Acrolein.

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15
Q

Mechlorethamine

A
  • Alkylating agent
  • Not excreted
  • Hodgkins’ disease
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16
Q

Cyclophosphamide

A
  • Alkylating agent
  • Must be activated by P450 in the liver
  • SIDAH (water intox)
  • Tx: Burkitt’s lymphoma, acute lymphocytic leukemia
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17
Q

Chlorambucil

A
  • Alkylating agent
  • Hepatotoxicity
  • Tx: Chronic lyphocytic leukemia
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18
Q

What is MESNA used for in cancer treatment therapy?

A
  • To decrease hemorrhagic cycstitis produced by acrolein.

- Prevents acrolein from binding to bladder wall

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19
Q

Estramustine phosphate

A
  • Combination of nitrogen mustard and estradiol
  • PO administration
  • In vivo binds to Beta-tubulin
  • Antimitotic effects
  • CCNS and M-phase
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20
Q

Busulfan

A
  • CCNS

- S/Es: Pulmonary fibrosis and hyperpigmentation

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21
Q

Nitrosoureas:

  • Carmustine (BCNU)
  • Lomustine (CCNU)
  • Semustine (Methyl-CCNU)
  • Streptozotocin
A
  • CCNS
  • Lipophilic = pass blood/brain barrier
  • S/Es: Pulmonary fibrosis and nephrotoxicity
  • Breakdown in vivo to liberate alkylating and carbamylating species
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22
Q

Procarbazine

A
  • CCNS
  • Decreases DNA, RNA and protein synthesis
  • Inhibits transition from G1 to S phase
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23
Q

Dacarbazine (DTIC)

Temozolomide

A
  • CCNS
  • Methylate DNA and RNA
  • Prevents transcription and translation
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24
Q

Platinum Drugs:

  • Cisplatin
  • Carboplatin
  • Oxaliplatin
A
  • CCNS
  • Binds to guanine in DNA forming crosslinks
  • Interferes with DNA replication and mitosis
  • Triggers apoptosis
  • S/Es: Decreased BM, nephrotoxicity, peripheral neuropathy, ototoxicity
  • Must check kidney function
  • Tx with loop diuretics (furosemide)
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25
Q

Anthracyclines:

  • Doxorubicin
  • Daunorubicin
A
  • CCNS
  • Inhibits transcription and replication
  • Blocks topoisomerase II
  • S/E: Cardiotoxicity
    • May be prevented by dexrazoxane
26
Q

Epipodophyllotoxins:

  • Etoposide
  • Tenopside
A
  • Kills in S and G2 phases
  • Forms ternary complex with DNA and topoisomerase II
  • Causes breakage of DNA strands
27
Q

Camptothecin Analogs:

  • Camptothecin
  • Topotecan
  • Irinotecan
A
  • Act in S phase
  • Irinotecan is a prodrug
  • Binds to the topoisomerase I and DNA complex
  • Prevents DNA replication
  • Severe diarrhea possible
28
Q

Bleomycins

A
  • Active in G2 phase
  • Bind to reduced iron in cells and lead to free radical production
  • S/Es: Pulmonary fibrosis, pneumonitis, cutaneous reactions, low grade fever, minimal BM suppression
29
Q

Dactinomycin

A
  • CCNS
  • Prevents DNA transcription
  • Most potent known
  • S/Es: Oral and GI ulceration, stomatitis
30
Q

Folic Acid Analogs:

  • Methotrexate (MTX)
  • Trimetrexate (lipid soluble)
  • Pemetrexed (multitargeted)
A
  • Active in S phase
  • Blocks the biosynthesis of purines
  • Decreases DNA synthesis
  • S/Es: Oral and GI ulceration, hepatotoxicity, pulmonary toxicity
31
Q

Leucovorin

A
  • Administered 24-36 hrs after MTX

- Bypass the metabolic block of MTX

32
Q

Fluorouracil

A
  • CCNS
  • Decreased DNA synthesis
  • S/Es: Oral and GI ulceration; stop at earliest signs of stomititis and diarrhea
33
Q

Cytarabine

A
  • Active in S phase
  • Inhibits DNA polymerase alpha
  • Oral ucleration
34
Q

Gemcitabine

A
  • CCNS

- Inhibits DNA synthesis

35
Q

What is the active form of 5-FU? What does it inhibit?

A
  • 5-FdUMP

- Inhibits action of thymidyate synthase

36
Q

Mercaptopurine (6-MP)

A
  • Inhibits synthesis of adenine and guanine
  • Acts at S phase
  • Metabolism inhibited by allopurinol
  • S/Es: Cholestasis; oral and intestinal ulcers
37
Q

Thioguanine (6-TG)

A
  • Acts in S phase

- Inhibits synthesis of purines

38
Q

Adenosine Deaminase Inhibitors:

  • Pentostatin
  • Cladribine
  • Fludarabine
A
  • Inhibit adenosine deaminase

- Decreases DNA synthesis

39
Q

Vinca alkaloids:

  • Vincristine
  • Vinblastine
  • Vinorelbine
A
  • Acts in M-phase
  • Bind to soluble tubulin, blocks polymerization and arrests cellular mitosis in metaphase
  • S/Es: Peripheral neuropathy, alopecia, nephrogenic SIADH
40
Q

Yew alkaloids:

  • Paclitaxel
  • Docetaxel
A
  • Acts in M phase
  • Prevents microtubule depolymerization, cells are arrested in late G2 or M phase
  • S/Es: Peripheral neuropathy = dose limiting
41
Q

L-Asparaginase

A
  • Catalyzes conversion of L-asparagine
  • Inhibits RNA and DNA synthesis
  • S/Es: Increased risk for thrombosis, impaired liver function, kidney or CNS.
42
Q

Mitotane

A
  • CCNS
  • Blocks hormone production by the adrenal gland
  • Destroys adrenal and cancer cells
  • S/Es: Fatigue and nausea
43
Q

Interferons

A
  • CCNS
  • Inhibits tumors by regulating the host immune system of the pt
  • Slows G1–>S; S–>G2
44
Q

Prednisone

A
  • Anti-inflammatory

- Apoptosis in certain leukemic cells

45
Q

Progestins

A

-Used in hormone responsive cancers expressing progesterone receptor

46
Q

Tamoxifen, Toremefine

A
  • Antiestrogens

- Used in estrogen receptor positive breast cancer.

47
Q

Anti-androgens

A
  • Blocks androgen-induced growth
  • Normally combined with leuprolide or other luteinizing hormone releasing hormone agonist
  • Anti-androgens + leuprolide = total androgen ablation
48
Q

Bevaczimab

A

-Blocks VGEF and prevents angiogenesis

49
Q

Denusomab

A

-Blocks RANK-RANKL in bone

50
Q

Trastuzumab

A

-Blocks Her2/C-Neu

51
Q

Ipilimumab

A
  • Blocks CTLA4

- S/Es: Colitis

52
Q

Tremelimumab

A
  • Blocks CTLA4

- S/Es: Diarrhea, colitis, skin rash

53
Q

Nivolumab

A
  • Blocks PD-1

- S/Es: Fatigue, colitis, skin rash

54
Q

Pembrolisumab

A
  • Blocks PD-1

- Fatigue, skin rash

55
Q

Imatinib

A

Blocks Bcr-Abl Kinase

56
Q

Erlotinib, Gefitinib

A

-Blocks EGFR signaling

57
Q

Crizotinib

A

-Blocks ALK-1 kinase

58
Q

Amirubicin

A
  • Anthracyline

- Reduced cardiotoxicity

59
Q

Fulvestrant

A
  • ER blocker
  • Lacks partial estrogen activity
  • Useful for estrogen responsive cancers
60
Q

Abraxane

A
  • IV nanoparticle
  • Albumin bound formulation of paclitaxel
  • Cremophor-free
61
Q

Picoplatin

A
  • Organic platinum containing

- Does not cause platinum resistance

POD III (12 decks)

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