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Hematology - Pharmacology > Onc drugs > Flashcards

Onc drugs Flashcards

1
Q

What class of drug is azathioprine, 6-MP/6-TG?

A

Anti-metabolite

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2
Q

What is the mechanism of action of azathioprine, 6-MP/6-TG?

A
  1. Purine (thiol) analogs decrease de novo purine synthesis.
  2. Activated by HGPRT
  3. Azathioprine is metabolized to 6MP.
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3
Q

What is the clinical use for azathioprine, 6-MP/6-TG?

A 
Preventing organ rejection, 
rheumatoid arthritis, IBD, 
SLE; used to wean patients 
off steroids in chronic disease 
and to treat steroid-refractory 
chronic disease.
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4
Q

What is the toxicity of azathioprine, 6-MP/6-TG?

A

Myelosuppression, GI, liver.

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5
Q

What drugs do azathioprine etc have increased risk of toxicity with and why?

A

allopurinol or febuxostat, because metabolized by xanthine oxidase.

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6
Q

What class of drug is cladribine (2-CDA)?

A

Antimetabolite

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7
Q

What is the mechanism of action of cladribine?

A

Purine analog, multiple
mechanisms (e.g., inhibition
of DNA polymerase, DNA
strand breaks).

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8
Q

What is the clinical use of cladribine?

A

Hairy cell leukemia.

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9
Q

What are the toxicities of cladribine?

A

Myelosuppression,
nephrotoxicity, and
neurotoxicity.

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10
Q

What drug class is cytarabine (arabinofurosyl cytidine)?

A

Pyrimidine analog –> inhibition of DNA polymerase.

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11
Q

What is the clinical use for cytarabine (arabinofurosyl cytidine?

A

Leukemias (AML), lymphomas

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12
Q

What are the toxicities of cytarabine (arabinofurosyl cytidine?

A 
Leukopenia, 
thrombocytopenia, 
megaloblastic anemia. 
(CYTarabine causes 
panCYTopenia.)
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13
Q

What drug class is 5-FU?

A

antimetabolite

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14
Q

What is the mechanism of action of 5-FU?

A 
Pyrimidine analog bioactivated 
to 5F-dUMP, which 
covalently complexes folic 
acid. This complex inhibits 
thymidylate synthase 
, resulting in decr dTMP Ž and decr DNA 
synthesis.
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15
Q

What is the clinical use of 5-FU?

A

Colon cancer, pancreatic
cancer, basal cell carcinoma
(topical).

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16
Q

What are the toxicities of 5-FU?

A

Myelosuppression, which is
not reversible with leucovorin
(folinic acid).

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17
Q

What drug class is methotrexate?

A

Antimetabolite

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18
Q

What is the mechanism of action of methotrexate?

A

Folic acid analog that
competitively inhibits
dihydrofolate reductase, decreasedTMP Žand decreaseDNA
synthesis.

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19
Q

What drug class is bleomycin?

A

Anti-tumor antibiotic

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20
Q

What is the mechanism of action of bleomycin?

A

Induces free radical formation –> breaks in DNA strands.

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21
Q

What is the clinical use of bleomycin?

A

Testicular cancer, Hodgkin’s lymphoma.

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22
Q

What is the toxicity associated with bleomycin?

A

Pulmonary fibrosis, skin hyperpigmentation,

mucositis. Minimal myelosuppression

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23
Q

What drug class is dactinomycin/actinomycin D?

A

Anti-tumor antibiotic.

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24
Q

What is the mechanism of action of dactinomycin/actinomycin D?

A

Intercalates in DNA - binds DNA at the transcription site and won’t let go.

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25
Q

What is the clinical use of dactinomycin/actinomycin D?

A

Childhood tumors - wilms tumor, ewiing sarcoma, rhabdomyosarcoma.

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26
Q

What is the toxicity associated with dactinomycin/actinomycin D?

A

Myelosuppresion.

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27
Q

What drug class is doxorubiin/daunorubicin?

A

Generates free radials, intercalates in DNA, breaks in DNA, decr replication

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28
Q

What is the clinical use of doxorubicin/daunorubicin?

A

Solid tumors, leukemias, lymphomas

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29
Q

What is the toxicity assoicated with doxorubicin/daunorubicin?

A 
Cardiotoxicity (dilated 
cardiomyopathy), 
myelosuppression, alopecia. 
Toxic to tissues following 
extravasation.
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30
Q

What is used to prevent cardiotoxicity of doxorubicin?

A

Dexrazone (iron chelating agent).

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31
Q

What drug class is busulfan?

A

Alkylating agent

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32
Q

What is the mechanism of busulfan?

A

Cross-links DNA

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33
Q

What is the clinical use of busulfan?

A

CML. Also used to ablate patient’s bone marrows before transplantation.

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34
Q

What is the toxicity of busulfan?

A 
Severe myelosuppression (in 
almost all cases), pulmonary 
fibrosis, hyperpigmentation.
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35
Q

What drug class is cyclophosphamide/ifosphamide?

A

Alkylating agents

36
Q

What is the mechanism of cyclophosphamide/ifosphamide?

A

Cross-link DNA at guanine
N-7. Require bioactivation by
liver.

37
Q

What is the clinical use of cyclophosphamide/ifosphamide?

A

Solid tumors, leukemia, lymphoma

38
Q

What is the toxicity of cyclophosphamide/ifosphamide?

A 
Myelosuppression; 
hemorrhagic cystitis, partially 
prevented with mesna (thiol 
group of mesna binds toxic 
metabolites).
39
Q

What is the drug class of the nitrosoureas?

A

Alkylating agents

40
Q

What are carmustine, lomustine, semustine, and streptozicin?

A

nitrosoureas

41
Q

What is the mechanism of action of nitrosoureas?

A

Require bioactivation.
Cross blood-brain barrier
Ž CNS. Cross-link DNA.

42
Q

What is the clinical use of nitrosoureas?

A

Brain tumors incl GBM.

43
Q

What are the toxicities of nitrosoureas?

A

CNS toxicity - convulsions, dizziness, ataxia.

44
Q

What drug class is paclitaxel/other taxols?

A

Microtubule inhibitors

45
Q

What is the mechanism of action of paclitaxel?

A 
Hyperstabilize polymerized 
microtubules in M phase so 
that mitotic spindle cannot 
break down (anaphase cannot 
occur).
46
Q

What is the clinical use of paclitaxel?

A

Ovarian and breast carcinoma.

47
Q

What are the toxicities of paclitaxel?

A

Myelosuppression, alopecia,

hypersensitivity.

48
Q

What drug class is vincristine/vinblastine?

A

Vinca alkyloids/microtubule inhibitors.

49
Q

What is the mechanism of action of vincristine/vinblastine?

A 
Vinca alkaloids that bind 
β-tubulin and inhibit 
its polymerization into 
microtubules Ž prevent 
mitotic spindle formation 
(M-phase arrest).
50
Q

What is the clinical use of vincristine/vinblastine?

A 
Solid tumors, leukemias, 
Hodgkin (vinblastine) and 
non-Hodgkin (vincristine) 
lymphomas.
(blast the owl).
51
Q

What are the toxicities of vincristine/vinblastine?

A 
Vincristine: neurotoxicity 
(areflexia, peripheral neuritis), 
paralytic ileus.
Vinblastine blasts bone 
marrow (suppression).
52
Q

What is the mechanism of cisplatin/carboplatin?

A

Cross-link DNA.

53
Q

What is the clinical use of cisplatin/carboplatin?

A

Testicular, bladder, ovary, and lung carcinomas.

54
Q

What are the toxicities of cisplatin/carboplatin?

A

Nephrotoxicity, ototoxicity.

55
Q

What can be used to prevent cisplatin/carboplatin nephrotoxicity?

A

Prevent nephrotoxicity with amifostine (free radical scavenger) and
chloride (saline) diuresis.

56
Q

What is the mechanism of etoposide/teniposide?

A

Etoposide inhibits topoisomerase II; Incr DNA degradation.

57
Q

What is the clinical use of etoposide/teniposide?

A

Solid tumors (particularly testicular and small cell lung cancer), leukemias, lymphomas.

58
Q

What are the toxicities of etoposide/teniposide?

A

Myelosuppression, GI upset, alopecia.

59
Q

What is the mechanism of irinotecan/topotecan?

A

Inhibit topoisomerase I and prevent DNA unwinding and replication.

60
Q

What is the clinical use of irinotecan/topotecan?

A

Colon cancer (irinotecan); ovarian and small cell lung cancers (topotecan).

61
Q

What are the toxicities of irinotecan/topotecan?

A

Severe myelosuppression, diarrhea.

62
Q

What is the mechanism of hydroxyurea?

A

Inhibits ribonucleotide reductase ; Decrease DNA Synthesis (S-phase specific).

63
Q

What is the clinical use of hydroxyurea?

A

Melanoma, CML, sickle cell disease ( HbF).

64
Q

What are the toxicities of hydroxyurea?

A

Severe myelosuppression, GI upset.

65
Q

What is the mechanism of action of prednisone/prednisolone?

A

Various; bind intracytoplasmic receptor; alter gene transcription.

66
Q

What are the clinical uses of prednisone/prednisolone?

A

Most commonly used glucocorticoids in cancer chemotherapy. Used in CLL, non-Hodgkin
lymphoma (part of combination chemotherapy regimen). Also used as immunosuppressants (e.g.,
in autoimmune diseases).

67
Q

What are the toxicities of prednisone/prednisolone?

A

Cushing-like symptoms; weight gain, central obesity, muscle breakdown, cataracts, acne,
osteoporosis, hypertension, peptic ulcers, hyperglycemia, psychosis.

68
Q

What is the mechanism of bevacizumab?

A

Monoclonal antibody against VEGF. Inhibits angiogenesis.

69
Q

What are the clinical uses of bevacizumab?

A

Solid tumors (colorectal cancer, renal cell carcinoma).

70
Q

What are the toxicities of bevacizumab?

A

Hemorrhage, blood clots, and impaired wound healing.

71
Q

What is the mechanism of erlotinib?

A

EGFR tyrosine kinase inhibitor.

72
Q

What are the clinical uses of erlotinib?

A

Non-small cell lung carcinoma.

73
Q

What are the toxicities of erlotinib?

74
Q

What is the mechanism of imatinib?

A

Tyrosine kinase inhibitor of BCR-ABL (Philadelphia chromosome fusion gene in CML) and c-kit
(common in GI stromal tumors).

75
Q

What are the clinical uses of imatinib?

A

CML, GI stromal tumors.

76
Q

What are the toxicities of imatinib?

A

Fluid retention.

77
Q

What is the mechanism of rituximab?

A

Monoclonal antibody against CD20, which is found on most B-cell neoplasms

78
Q

What are the clinical uses of rituximab?

A

Non-Hodgkin lymphoma, CLL, IBD, rheumatoid arthritis.

79
Q

What are the toxicities of rituximab?

A

Incr risk of progressive multifocal leukoencephalopathy.

80
Q

What is the mechanism of tamoxifen/raloxifene?

A

Selective estrogen receptor modulators (SERMs)—receptor antagonists in breast and agonists in
bone. Block the binding of estrogen to ER
⊕ cells.

81
Q

What are the clinical uses of tamoxifen/raloxifene?

A

Breast cancer treatment (tamox only) and prevention. Raloxifene also useful to prevent osteoporosis.

82
Q

What are the toxicities of tamoxifen/raloxifene?

A

Tamoxifen—partial agonist in endometrium, which  the risk of endometrial cancer; “hot flashes.”
Raloxifene—no  in endometrial carcinoma because it is an estrogen receptor ANTAGONIST in
endometrial tissue.

83
Q

What is the mechanism of trastuzumab?

A

Monoclonal antibody against HER-2 (c-erbB2), a tyrosine kinase receptor.
Helps kill cancer cells
that overexpress HER-2, through inhibition of HER2-initiated cellular signaling and antibody-dependent cytotoxicity.

84
Q

What are the clinical uses of trastuzumab?

A

HER-2⊕ breast cancer and gastric cancer (tras2zumab).

85
Q

What are the toxicities of trastuzumab?

A

Cardiotoxicity. “Heartceptin” damages the heart.

86
Q

What is the mechanism of vemurafenib?

A

Small molecule inhibitor of BRAF oncogene

⊕ melanoma

87
Q

What is the clinical use of vemurafenib?

A

Metastatic melanoma

Hematology - Pharmacology (2 decks)

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