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Pharm > CHEMOTHERAPY OF NEOPLASTIC DISEASES 3 > Flashcards

CHEMOTHERAPY OF NEOPLASTIC DISEASES 3 Flashcards

1
Q

Who are the vinca alkaloids and what do they do

A

Vincristine
Vinblastine

  • Destabilizing agents.
  • Vinca alkaloids bind to β-tubulin and inhibit its ability to polymerize into microtubules.
  • This results in mitotic arrest in metaphase.
  • Cell division stops. Cells die by apoptosis.
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2
Q

Adverse effects of vincristine

A
  • Peripheral neuropathy.*****
  • Bone marrow depression is mild.
  • Alopecia.
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3
Q

Adverse effects of vinblastine

A

• Myelosuppression is the dose-limiting
adverse effect.*****
• Peripheral neuropathy
• Alopecia

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4
Q

Example of a taxane and its MOA

A

Paclitaxel

  • Stabilizing agent.
  • Taxanes bind to the β-tubulin subunit of microtubules and promote microtubule polymerization.
  • Stabilization of the microtubules in a polymerized state arrests cells in mitosis and leads to apoptosis.
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5
Q

TAXANES: ADVERSE EFFECTS

A

• Hypersensitivity, myelosuppression, peripheral neuropathy, alopecia.

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6
Q

How to reduce hypersensitivity from taxane

A

by premedication with dexamethasone, diphenhydramine and an H2 blocker

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7
Q

EPIPODOPHYLLOTOXINS:

ETOPOSIDE MOA

A

Inhibits topoisomerase II, resulting in DNA damage through strand breakage.

Blocks cell in late S-G2 phase

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8
Q

What are the adverse effects of etoposide

A
  • Nausea, vomiting, alopecia.

* Myelosuppression.

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9
Q

Which drugs are camptothecins and what is their MOA

A

TOPOTECAN
IRINOTECAN

Inhibit topoisomerase I. Inhibition results in DNA damage.

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10
Q

Adverse effects of camptothecins

A

Myelosuppression and diarrhea

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11
Q

Which glucocorticoid is used and what is it used for

A

PREDNISONE
• Glucocorticoids are lympholytic and suppress mitosis in lymphocytes.
• They are used for acute leukemia and malignant lymphomas.

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12
Q

Who are the estrogen inhibitors

A
  • SELECTIVE ESTROGEN-RECEPTOR MODULATORS (SERMs)
  • ESTROGEN-RECEPTOR ANTAGONISTS
  • AROMATASE INHIBITORS (AIs)
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13
Q

Who are your SERMS AND what do they do

A

TAMOXIFEN
RALOXIFENE

• SERMs bind to estrogen receptors and act as agonists or antagonists depending on the tissue.

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14
Q

What is tamoxifen used for

A
  • Metastatic breast cancer in women and men.

* Preventive agent in women at risk for breast cancer.

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15
Q
  • Tamoxifen is an ____________ on breast tissue.

* Tamoxifen is an ____________ in nonbreast tissues.

A
  • Tamoxifen is an antagonist on breast tissue.

* Tamoxifen is an agonist in nonbreast tissues.

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16
Q

ADVERSE EFFECTS of tamoxifen

A
  • Hot flashes. Nausea. Vomiting. Fluid retention.
  • Vaginal bleeding.
  • Venous thromboembolism.
  • Increases incidence of endometrial cancer**
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17
Q

Tamoxifen is metabolized by CYP2D6 so it needs to stay away from Strong inhibitors of CYP2D6. Or else there would be accumulation . Who are Strong Inhibitors of CYP2D6?

A

Bupropion Fluoxetine Paroxetine

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18
Q

What is raloxifene used for ?

A
  • Prophylaxis of breast cancer in high-risk postmenopausal women. (Anti estrogen effect)
  • Treatment and prevention of osteoporosis in postmenopausal women. (Estrogenic effect)
19
Q

Adverse effects of raloxefine

A
  • Hot flashes.
  • Leg cramps.
  • Venous thromboembolism.
20
Q

Who is the estrogen antagonist

A

FULVESTRANT
• Fulvestrant is devoid of estrogen agonist activity.
• Fulvestrant binds to the estrogen receptor (ER) inhibits its dimerization and increases its degradation.
• ER-mediated transcription is abolished.

21
Q

Which drug is the Treatment of hormone receptor positive metastatic breast cancer in postmenopausal women with disease progression following antiestrogen therapy.

A

FULVESTRANT

22
Q

• Aromatase converts ______ to estrone.

A

• Aromatase converts androstenedione to estrone.

23
Q

Uses of aromatase inhibitors

A

the standard of care for adjuvant treatment of postmenopausal women with hormone receptor–positive breast cancer.

24
Q

Who are the non steroidal aromatase inhibitors

A

ANASTROZOLE & LETROZOLE
• Nonsteroidal.
• Reversible competitive inhibitors of aromatase.

25
Q

Who are the steroidal aromatase inhibitors

A

Steroidal

Inverse inhibitor of aromatase

26
Q

Who are the GONADOTROPIN-RELEASING HORMONE AGONISTS

A

GOSERELIN
LEUPROLIDE

Synthetic analogs of gonadotropin-releasing hormone.
• When given continuously or as a depot preparation, they cause an initial surge in LH and FSH levels, resulting in a transient increase in circulating gonadal steroids, followed by inhibition of gonadotropin release.

This results in reversible suppression of ovarian and testicular steroidogenesis.

27
Q
  • Testosterone levels fall to 10% of their initial values after a month with GnRH analogs.
  • But they increase in the beginning, causing a transient flare of tumor activity and an increase in symptoms.
  • The flare phenomenon can be counteracted with?
A

Flutamide

28
Q

GONADOTROPIN-RELEASING HORMONE AGONISTS USES:

A
  • Advanced carcinoma of the prostate. Alone or in combination with flutamide.
  • Advanced breast cancer in premenopausal women.
  • Management of endometriosis.
29
Q

Flutamide MOA

A
  • Synthetic, nonsteroidal antiandrogen.
  • Metabolized to an active metabolite that acts as a competitive antagonist at the androgen receptor, preventing its translocation to the nucleus.
30
Q

MOA of gefitinib and erlotinib

A

Inhibitors of the EGFR tyrosine kinase.

31
Q

What does lapatinib do

A

Inhibitor of EGFR and Her2 tyrosine kinases.

32
Q

Which drug is an Inhibitor of the tyrosine kinase of Bcr-Abl?

A

Imatinib

Used for Ph+ Chronic Myeloid Leukemia Ph+ Acute Lymphoblastic Leukemia
Myelodysplastic/ Myeloproliferative Diseases

33
Q

Who is the first line drug for Breast cancer with HER2 over-expression and what does it do

A

Trastuzumab - Monoclonal antibody against Her2.

34
Q

Which drug is used for the following

Metastatic colorectal cancer
Non-small cell lung cancer
Glioblastoma multiforme
Renal cell carcinoma

A

Bevacizumab- monoclonal antibody against VEGF

35
Q

ASPARAGINASE MOA

A

Asparaginase hydrolyzes serum asparagine, depriving these cells of the asparagine necessary for protein synthesis, leading to cell death.

36
Q

ASPARAGINASE: ADVERSE EFFECTS

A
  • Hypersensitivity.
  • Decrease in clotting factors.
  • Liver abnormalities.
  • Pancreatitis, seizures, coma due to ammonia toxicity.
37
Q

Which drug inhibits ribonucleotide reductase leading to depletion of deoxynucleoside
trisphosphate pools?

A

Hydroxyurea

It inhibits dna synthesis and kills cells in S phase .

38
Q

Which drug is Approved for hairy cell leukemia, chronic myelogenous leukemia (CML), malignant melanoma and Kaposi’s sarcoma.

A

Interferon alpha

39
Q

DOC for brain cancer

A

Lomustine, Carmustine

40
Q

DOC for Breast:

Hormone receptor-positive

A

Aromatase inhibitor
Tamoxifen
Fulvestrant
GnRH agonists

41
Q

Breast:

Tumors overexpressing HER2

A

Trastuzumab

42
Q

Doc for prostate cancer

A

GnRH agonist ± flutamide

43
Q

Cisplatin is the DOC for which three cancers

A

Ovarian
Testicular
Lung

44
Q

DOC for colorectal cancer

A

Fluorouracil + leucovorin

Pharm (8 decks)

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