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Hematology And Oncology > Cancer Drugs > Flashcards

Cancer Drugs Flashcards

1
Q

8 antimetabolites drugs

A
  1. Azathioprine 2. Cladribine 3. Cytarabine 4. 5-fluorouracil 5. Hydroxyurea 6. Methotrexate 7. 6-mercaptopurine 8. 6-thioguanine
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2
Q

Azathioprine, 6-mercaptopurine, 6-thioguanine mechanism of action

A

Purine (thiol) analogs–> decrease de novo purine synthesis

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3
Q

Azathioprine, 6-mercaptopurine, 6-thioguanine are activated by

A

HGPRT

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4
Q

Azathioprine is metabolized into

A

6-MP

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5
Q

Azathioprine, 6-mercaptopurine, 6-thioguanine clinical use

A
  1. Prevent organ rejection
  2. RA. 3. SLE. 4. IBD. 5 wean patients off steroids in chronic disease
  3. Treat steroid-refractory chronic disease
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6
Q

Azathioprine, 6-mercaptopurine, 6-thioguanine side effects

A
  1. Myelosuppresion 2. GI. 3. Liver
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7
Q

Azathioprine and MP-6 are metabolized by

A

Xantine oxidase

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8
Q

Azathioprine and MP-6 has increased toxicity if administrated with

A
  1. Allopurinol
  2. Febuxostat
    (Both xanthine oxidase inhibitors,for lynch nyhan syndrome
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9
Q

Cladribine (2-CDA) mechanism of action

A

Purine analog –> inhibition of dna polymerase, dna strand breaks)

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10
Q

Cladribine (2-CDA) clinical use

A

Hairy cell leukemia

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11
Q

Cladribine (2-CDA) toxicity

A
  1. Myelosupression
  2. Nephrotoxicity
  3. Neurotoxicity
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12
Q

Cytarabine (arabinofuranosyl cytidine) mechanism of action

A

Pyrimidine analog –> Dna polymerase inhibitor

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13
Q

Cytarabine (arabinofuranosyl cytidine) clinical use

A

AML

LYMPHOMAS

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14
Q

Cytarabine (arabinofuranosyl cytidine) toxicity

A
  1. Leukopenia
  2. Thrombocytopenia
  3. Megaloblastic anemia
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15
Q

Methotrexate (MTX) mechanism of action

A

Folic acid analog that inhibits dihydropholate reductase–> decreases dTMP–>decreases DNA synthesis

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16
Q

Methotrexate (MTX) clinical use

A
  1. Cancers (ALL, lymphomas, choriocarcinoma, sarcomas)

2. Non-neoplastic: ectopic pregnant, medical abortion (with misoprostol), RA, psoriasis, IBD, vasculitis

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17
Q

Methotrexate (MTX) toxicity

A
  1. Myelosupression (REVERSIBLE WITH LEUCOVORIN)
  2. Hepatotoxicity
  3. Mucositis (mount ulcers)
  4. Pulmonary fibrosis
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18
Q

Antimetabolites drugs action

A

Inhibit DNA synthesis (S phase)

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19
Q

5-fluorouracil toxicity

A

Myelosupression (NOT REVERSIBLE WITH LEUCOVORIN)

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20
Q

5-fluorouracil clinical use

A
  1. Colon cancer
  2. Pancreatic cancer
  3. Basal cell carcinoma (topical)
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21
Q

5-fluorouracil mechanism of action

A

Pyrimidine analog bioactivated to 5F-dUMP which covalently complexes folic acid–> this complex inhibits thymidylate synthase –> decreased dTMP –> decreased DNA synthesis

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22
Q

Hydroxyurea mechanism of action

A

Inhibits ribonucleatide reductase

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23
Q

Antitumor antibiotics

A
  1. Bleomycin
  2. Dactinomycin (actinomycin D)
  3. Doxorubicin, daunorubicin
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24
Q

Bleomycin mechanism of action

A

Induce free radicals –> breaks in DNA strands

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25
Q

Bleomycin clinical use

A

Testicular cancer

Hodgkin lymphoma

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26
Q

Bleomycin side effects

A
  1. Pulmonary fibrosis
  2. MINIMAL myelosupression
  3. Skin hyperpigmentation
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27
Q

What part of cycle does bleomycin inhibit

A

G2 (double check repair)

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28
Q

Dactinomycin (actinomycin D) side effects

A

Myelosuppression

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29
Q

Dactinomycin (actinomycin D) mechanism of action

A

Intercalates in DNA

30
Q

Dactinomycin (actinomycin D) clinical use

A

Used for childhood tumors

  1. Wilms
  2. Ewing sarcoma
  3. Rhabdomyosacroma
31
Q

Doxorubicin,

Daunorubicin mechanism of action

A
  1. Generates free radicals

2. Intercalate in DNA–> breaks in DNA–> decreased replication

32
Q

Doxorubicin,

Daunorubicin clinical uses

A
  1. Solid tumors
  2. Leukemias
  3. Lymphomas
33
Q

Doxorubicin,

Daunorubicin side effects

A

Toxic to tissues following extravasation

  1. Dilated cardiomyopathy
  2. Alopecia
  3. Myelosuppression
34
Q

How to prevent dilated cardiomyopathy with doxorubicin or daunorubicin administration

A

Dexrazoxane, an iron chelatin agent

35
Q

Alkylating agents

A

Busulfan
Cyclophosphamide, isosfamide
Nitrosoureas (carmustine, iomustine, semustine, streptozocin)

36
Q

Busulfan mechanism of action

A

Cross-links DNA

37
Q

Busulfan clinical use

A
  1. CML

2. To ablate patient’s bonipe marrow before bone marrow transplantation

38
Q

Busulfan side effects

A
  1. Severe myelosuppression (almost always)
  2. Pulmonary fibrosis
  3. Hyperpigmentation
39
Q

Nitrosoureas toxicity

A

Cns: 1. Dizziness 2. Ataxia 3. Convulsion

40
Q

Nitrosoureas clinical use

A

Brain tumors (including glioblastoma multiforme)

41
Q

Nitrosoureas mechanism of action

A

Require bioactivation
Cross BBB
cross link DNA

42
Q

Cyclophosphamide, ifosfamide mechanism of action

A

Cross link DNA at guanine N-7

Require bioactivation by liver

43
Q

Cyclophosphamide, ifosfamide clinical use

A
  1. Solid tumors
  2. Leukemia
  3. Lymphomas
44
Q

Cyclophosphamide, ifosfamide toxicity

A
  1. Myelosuppresion

2. Hemorrhagic cystitis

45
Q

Partially Prevent hemorrhagic cystitis in Cyclophosphamide, ifosfamide by:

A

Mesna (thiol group of mesna binds toxic metabolitis)

46
Q

Microtubule inhibitors

A
  1. Paclitaxel, and others taxols
  2. Vincristine
  3. Vinblastine
47
Q

Paclitaxel toxicity

A
  1. Myelosuppression
  2. Alopecia
  3. Hypersensitivity
  4. Neuropathy
48
Q

Paclitaxel clinical use

A
  1. Ovarian ca

2. Breast ca

49
Q

Paclitaxel mechanism of action

A

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

50
Q

Vinblastine clinical use

A
  1. Solid tumor
  2. Leukemia
  3. Hodgkin
51
Q

Vincristine clinical use

A
  1. Solid tumor
  2. Leukemias
  3. Non-hodgkin
52
Q

Vincristine vs. vinblastine clinical uses

A

Both: solid tumor, leukemia
Vinblastine: Hodgkin
Vincristine: non-Hodgkin

53
Q

Vinblastin toxicity

A

Myelossupression

54
Q

Vincristine toxicity

A
  1. Neurotoxicity: (areflexia, peripheral neuritis)

2. Paralytic ileus

55
Q

Vincristine, vinblastine mechanism of action

A

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

56
Q

Hydroxyurea mechanism of action

A

Inhibits ribonucleotide reductase (inhibits dna synthesis-S phase)

57
Q

Vinca alkaloids

A

Vincristine

Vinblastine

58
Q

Hydroxyurea clinical use

A
  1. Melanoma
  2. CML
  3. Sickle cell anemia (increases HbF)
59
Q

Hydroxyurea toxicity

A
  1. SEVERE myelosuppression

2. GI upset

60
Q

Vemurafenib clinical use

A

Metastatic melanoma

61
Q

Vemurafenib mechanism of action

A

Small molecule inhibitor of BRAF oncogene (melanoma)

62
Q

BRAF oncogene is (+) in

A

MELANOMA

63
Q

Erlotinib toxicity

A

Rash

64
Q

Erlotinib clinical use

A

Non small cell lung carcinoma

65
Q

Erletonib mechanism of action

A

EGFR tyrosine kinase inhibitor

66
Q

Cetuximab - mechanism of action

A

Monoclonal antibody against EGFR

67
Q

Cetuximab - clinical use

A
  1. stage IV CRC (wild-typeKRAS)

2. head and neck cancer

68
Q

Cetuximab - adverse effects

A
  1. rash
  2. elevated LFTs
  3. Diarrhea
69
Q

Etoposide tenoposide toxicity

A
  1. Myelosuppression
  2. Gi upset
  3. Alopecia
70
Q

Irinotecan, topotecan toxicity

A
  1. Severe myelosuppression

2. Diarrhea

Hematology And Oncology (21 decks)

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