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PHARMACOLOGY > Onc Drugs (A) > Flashcards

Onc Drugs (A) Flashcards

1
Q

Mechanism:

Azathioprine

6-mercaptopurine

A

Purine (thiol) analog → decrease de novo purine synthesis

Activated by HGPRT

Azthioprine is metabolized into 6-MP

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2
Q

Clinical use:

Azathioprine

6-mercaptopurine

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

Adverse effects:

Azathioprine

6-mercaptopurine

A
  1. Myelosuppression
  2. GI disturbances - abd pain
  3. Hepatotoxicity - jaundice
  4. Increased toxicity with allopurinol or febuxostat
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4
Q

Mechanism: Cladribine

A

Purine analog → multiple mechanisms:

  • Inhibition of DNA polymerase
  • DNA strand breaks
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5
Q

Clinical use: Cladribine

A
  1. Hairy cell leukemia
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6
Q

Adverse effects: Cladribine

A
  1. Myelosuppression
  2. Nephrotoxicity
  3. Neurotoxicity
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7
Q

Mechanism: Cytarabine

A

Pyrimidine analog → inhibition of DNA polymerase

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8
Q

Clinical use: Cytarabine

A

Leukemias (AML)

Lymphomas

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9
Q

Adverse effects: Cytarabine

A
  1. Myelosuppression + megaloblastic anemia
  2. Pancytopenia
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10
Q

Mechanism: 5-fluorouracil

A

Pyrimidine analog bioactivated to 5-FdUMP, which covalently complexes with thymidylate synthase and folic acid

Complex inhibits thymidylate synthase → decreased dTMP → decreased DNA synthesis

Capecitabine is a prodrug with similar activity

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11
Q

Clinical use: 5-fluorouracil

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

Effects enhanced with addition of leucovorin

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12
Q

Adverse effects: 5-fluorouracil

A
  1. Myelosuppression
  2. Palmar-plantar erythrodysesthesia (hand-foot syndrome)
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13
Q

Mechanism: Methotrexate

A

Folic acid analog that competitively inhibits dihydrofolate reductase → decreased dTMP → decreased DNA synthesis

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14
Q

Clinical use: Methotrexate

A

Neoplastic

  1. Leukemias (ALL)
  2. Lymphomas
  3. Choriocarcinoma
  4. Sarcomas

Non-neoplastic

  1. Ectopic pregnancy
  2. Medical abortion (with misoprostol)
  3. RA
  4. Psorasis
  5. IBD
  6. Vasculitis
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15
Q

Adverse effects: Methotrexate

A
  1. Myelosuppression (reversible with leucovorin)
  2. Hepatotoxicity
  3. Mucositis (e.g., mouth ulcers)
  4. Pulmonary fibrosis
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16
Q

Mechanism: Capecitabine

A

Prodrug with similar acitvity as 5-FU

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17
Q

Mechanism: Bleomycin

A

Induce free radical formation → breaks in DNA strands

18
Q

Clinical use: Bleomycin

A

Testicular cancer

Hodgkin lymphoma

19
Q

Adverse effects: Bleomycin

A

Pulmonary fibrosis

Skin hyperpigmentation

MINIMAL myelosuppression

20
Q

Mechanism: Dactinomycin (actinomycin D)

A

Intercalates in DNA

21
Q

Clinical use: Dactinomycin (actinomycin D)

A

Wilms tumor

Ewing sarcoma

Rhabdomyosarcoma

(childhood tumors)

22
Q

Adverse effects: Dactinomycin (actinomycin D)

A

Myelosuppression

23
Q

Mechanism:

Doxorubicin

Daunorubicin

A

Generate free radicals

Intercalate in DNA → breaks in DNA → decrease DNA replication

24
Q

Clinical use:

Doxorubicin

Daunorubicin

A

Solid tumors

Leukemias

Lymphomas

25
Q

Adverse effects:

Doxorubicin

Daunorubicin

A

Cardiotoxicity (dilated cardiomyopathy) - prevent with dexrazoxane

Myelosuppression

Alopecia

26
Q

___ is used to prevent cardiotoxicity with doxorubicin

A

Dexrazoxane

27
Q

Mechanism: Busulfan

A

Cross-links DNA

28
Q

Clinical use: Busulfan

A

CML (mainstay treatment is Imatinib)

Ablate bone marrow prior to bone marrow transplantation

29
Q

Adverse effects: Busulfan

A

Severe myelosuppression (almost all cases)

Pulmonary fibrosis

Hyperpigmentation

30
Q

Mechanism:

Cyclophosphamide

Ifosfamide

A

Nitrogen mustard

Cross-link DNA at guanine N-7

Require bioactivation by liver

31
Q

Clinical use:

Cyclophosphamide

Ifosfamide

A

Solid tumors

Leukemia

Lymphomas

Cyclophosphamide

  • Granulomatosis with polyangiitis (Wegener’s granulomatosis)
  • Microscopic polyangiitis
32
Q

Adverse effects:

Cyclophosphamide

Ifosfamide

A

Myelosuppression

Hemorrhagic cystitis - preventied with mesna or N-acetylcysteine (bind toxic metabolites)

33
Q

Mechanism: Nitrosoureas

(-MUSTINE)

A

Require bioactivation

Cross BBB → CNS

Cross-link DNA

34
Q

Clinical use: Nitrosoureas

(-MUSTINE)

A

Brain tumors (including glioblastoma multiforme)

35
Q

Adverse effects: Nitrosoureas

(-MUSTINE)

A

CNS toxicity → convulsion, dizziness, ataxia

36
Q

Mechanism: Paclitaxel

Other taxols

A

Hyperstabilize polyerized microtubules in M phase → mitotic spindle cannot break down → anaphase cannot occur

37
Q

Clinical use: Paclitaxel

Other taxols

A

Ovarian and breast carcinomas

38
Q

Adverse effects: Paclitaxel

Other taxols

A

Myelosuppression

Neuropathy

Hypersensitivity

39
Q

Mechanism:

Vinblastine

Vincristine

A

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

40
Q

Clinical use:

Vinblastine

Vincristine

A

Solid tumors

Leukemias

Vinblastine → HL

Vincristine → NHL

41
Q

Adverse effects:

Vincristine

A

Neurotoxicity → areflexia, peripheral neuritis

Constipation (including paralytic ileus)

PHARMACOLOGY (33 decks)

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