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Pharmacology > Anticancer > Flashcards

Anticancer Flashcards

1
Q

cancer drugs overview

A
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2
Q

describe primary, adjuvent, and neoadjuvent chemotherapy

A
  • Primary: when neoplasms are disseminated and not amenable to surgery
  • Adjuvent: used to attack micrometastases following surgery and radiation
  • Neoadjuvent: Given prior to surgery to shrink the cancer
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3
Q

which cells are most sensitive to anticancer drugs?

A
  • rapidly dividing cells
    • buccal mucosa (stomatitis)
    • bone marrow (myelosuppression)
    • GI mucosa (nausea vomit)
    • hair cells (alopecia)
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4
Q

describe cell-cycle specific drugs

A
  • Exert action on cells traversing cell cycle, most effecting in hematologic malignancies, useful in high growth-fraction tumours
  • Antimetaboites (S-phase)
  • Bleomycin (G2-phase)
  • Camptothecins
  • Epipodophyllotoxins (late S-G2 phase)
  • Microtubule inhibitors (metaphase arrest)
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5
Q

describe cell-cycle nonspecific drugs

A
  • kill tumour cells whether they are cycling (more sensitive) or in Go resting phase, useful in low and high growth-fraction solid tumours
  • Alkylating agents (can cause treatment induced neoplasms)
  • Platinum coordination complexes
  • Antitumour antibiotics
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6
Q

list high, medium, and low myelosuppression drugs

A
  • High
    • Cytarabine
    • Alkylating Agents
    • Doxorubucin and Daunorubucin (antitumour anitbiotic)
    • Vinblastine (vinca alkaloid)
  • Medium
    • Carboplatin
    • Methotrexate (antimetabolite)
    • 5-fluorouracil (antimetabolite)
  • Low
    • Bleomycin (antitumour anitbiotic)
    • Vincristine (vinca alkaloid)
    • Asparaginase
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7
Q

doxorubicin toxicity

A

cardiotoxicity - anticancer antibiotic

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8
Q

cyclophosphamide toxicity

A

hemorrhagic cystitis

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9
Q

bleomycin toxicity

A

pulmonary fibrosis

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10
Q

vincristine and paclitaxel toxicity

A

peripheral neuropathy

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11
Q

rescues bone marrow from methotrexate (methotrexate antidote)

A

Leucovorin

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12
Q

reduces hemorrhagic cystitis from cyclophosphamide

A

Mesna

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13
Q

reduces anthracycline-induced cardiotoxicity (ex. from doxorubicin)

A

Dexrazoxane

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14
Q

reduces renal toxicity caused by cisplatin

A

Amifostine

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15
Q

list antimetabolites and the phase it acts on

A
  • S-phase
  • folate analog: Methotrexate
  • purine analogs: 6-mercaptopurine (6-MP), 6-thioguanine (6-TG)
  • pyrimidine analogs: 5-fluorouracil (5-FU), Capecitabine, Cytarabine
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16
Q

Methotrexate MOA

A

Inhibits DHF reductase → deprives cells of folate → dTMP and purine nucleotide synthesis decreases → RNA/DNA/protein synthesis decreases → cell death

Undergoes conversation to a series of polyglutamates (MTX-PGs)

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17
Q

methotrexate AEs

A
  • Renal damage (from high-dose)
  • Hepatic fibrosis
  • Cirrhosis, pneumonitis, neurologic toxicities (IT administration)
  • Common: stomatitis, mucositis, myelosuppression, alopecia, nausea, vomiting
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18
Q

Leucovorin MOA

A
  • N5-formyl-THF
  • antidote for drugs that decrease folic acid (like methotrexate)
  • rescues bone marrow
  • provides normal tissues with reduced folate, circumventing the inhibition of DFHR
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19
Q

Clinical use of Leucovorin

A
  1. Rescues bone marrow suppression from MTX
  2. Potentiates effect of 5-FU
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20
Q

effects of Allopurinol

A

Potentiates 6-MP

No effect on 6-TG

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21
Q

6-Thioguanine treats which cancer specifically?

A

Acute nonlymphocytic leukemia

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22
Q

6-Mercaptopurine MOA

A

Converted to thio-IMP by HGPRT (purine salvage pathway) → inhibits 1st step of de novo purine synthesis
Thio-IMP also blocks formation of AMP and GMP
Dysfunctional RNA and DNA result from incorporation of guanylate analogs

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23
Q

xanthine oxidase

A

Metabolizes 6-MP to thioruic acid

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24
Q

If ___ is given to reduce ___, dose of 6-MP must be DECREASED to avoid accumulation

A

If allopurinol is given to reduce hyperuricemia, dose of 6-MP must be DECREASED to avoid accumulation

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25
Q

6-MP and 6-TG AEs

A
  • Nausea, vomiting, diarrhea
  • bone marrow suppression,
  • hepatotoxicity (6-MP)
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26
Q

6-thioguanine (6-TG) MOA

A

converted to nucleotide → inhibits purine synthesis and phosphorylation of GMP to GDP, can be incorporated into RNA and DNA

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27
Q

5-FU inhibits ___ resulting in ____.

A

5-FU inhibits thymidylate synthase resulting in ‘thymineless death’.

28
Q

Combination chemotherapy used for colorectal cancer

A

5-FU and LEUCOVORIN

Leucovorin increases N5,N10-methylene-THF, potentiating 5-FU (which inhibits thymidylate synthase)

29
Q

5-FU and Capecitabine AEs

A
  • HAND-FOOT SYNDROME: erythematous desquamation of the palms and soles seen after extended infusions
30
Q

Cytarabine (ARA-C) MOA

A

(deoxycytidine analog)

phosphorylated to triphosphate → incorporated into DNA → inhibits DNA polymerase

“tara takes double penetration”

31
Q

Antitumour Antibiotics MOA

A
  • Bind to DNA through INTERCALATION between bases and block synthesis of new RNA or DNA
  • causes DNA strand breakage and interferes with cell replication
  • Cell-Cycle NON specific agents
  • Bleomycin, Doxorubicin, Daunorubicin
32
Q

Doxorubicin & Daunorubicin MOA

A
  1. Inhibition of topoisomerase II
  2. intercalation in DNA with consequent blockade of DNA & RNA synthesis and strand breakage
  3. Binding to cell membrane to alter fluidity and ion transport
  4. Generation of free radicals (cause of cardiac toxicity)
33
Q

___ is an iron-chelating agent educing cardiotoxicity from ____

A

Dexrazoxane is an iron-chelating agent educing cardiotoxicity from Doxorubicin

34
Q

Bleomycin cell specific phase it acts on

A

G2 phase

35
Q

Alkylating Agents MOA

A
  • Cytotoxic effects via transfer of their alkyl groups to various cellular constituents leading to cell death
  • can occur on single strand or both strands through cross-linking
  • Nitrogen mustards, Nitrosoureas, Platinum coordination complexes, Busulfan, Dacarbazine, Procarbazine
36
Q

Alkylating Agents AEs

A
  • MUTAGENIC + CARCINOGENIC
  • particularly in rapidly growing tissues
37
Q

list the Nitrogen Mustards

A

mechlorethamine, cyclophosphamide, melphalan

(“MCM = Mel Phalan”)

38
Q

____ is a metabolite of cyclophosphamide, responsible for _____.

A

Acrolein is a metabolite of cyclophosphamide, responsible for hemorrhagic cystitis.

39
Q

list ways of preventing hemorrhagic cystitis

A
  • adequate fluid intake
  • mesna
  • acrolein
40
Q

list Nitrosoureas and its properties

A
  • Carmustine, Lomustine
  • very lipophilic, can cross BBB
  • useful treatment for BRAIN tumours
41
Q

Busulfan toxicity

A

Pulmonary fibrosis, myelosuppression

42
Q

____ is converted by liver P450 enzymes to alkylating metabolites

A

Procarbazine is converted by liver P450 enzymes to alkylating metabolites

43
Q

Procarbazine AEs

A
  • BONE MARROW DEPRESSION, nausea, vomiting
  • WEAK MAO INHIBITOR: hypertensive reactions may result if given with sympathomimetic agents, or tyramine-containing foods (cheese and wine)
  • DISULFIRAM-LIKE REACTIONS
  • mutagenic + teratogenic
44
Q

Cisplatin, Carboplatin MOA

treatment for which cancers?

A
  • Platinum drugs
  • Do not alkylate DNA
  • Covalently bind to DNA and CROSS-LINKS DNA
  • Broad antineoplastic activity
  • Treats: testicular cancer, ovarian cancer, and cancers of the head and neck, bladder, esophagus, lung and colon
45
Q

Cisplatin AEs

A
  • Nephrotoxicity, ototoxicity
  • Peripheral neuropathy
  • Mild/Moderate Myelosuppresion
46
Q

Carboplatin AEs

A
  • less nausea, neurotoxicity, ototoxicity, nephrotoxicity than cisplatin
  • dose-limiting toxicity is myelosuppression
47
Q

Vinca alkaloids/mictotubule inhibitors

A

Vicristine, vinblastine

48
Q

Vicristine, vinblastine (Vinca alkaloids) MOA

A
  • bind to B-tubulin and inhibits polymerization of microtubules
  • Arrest in M phase
  • Cell division stops → apoptosis
49
Q

Vinca Alkaloids AE

A
  • Vincristine: peripheral neuropathy
  • Vinblastine: dose-limiting myelosuppresion
50
Q

list the taxanes and their MOA

A
  • Paclitaxel, Docetaxel
  • Bind to B-tubulin of microtubules and promote microtubule polymerization
  • stabilization of microtubules arrests cells in mitosis → apoptosis
51
Q

Paclitaxel AEs

A
  • Hypersensitivity
  • peripheral neuropathy
52
Q

Hypersensitivity from Paclitaxel is reduced by premedication with…

A

Dexamethason, Diphenydramine, H2 blocker

53
Q

Docetaxel Adverse Effects

A
  • fluid retention
  • peripheral neuropathy (not as frequently as paclitaxel)
  • Myelosuppression is dose-limiting
54
Q

pretreatment with ____ is required to prevent fluid retention from docetaxel

A

pretreatment with Dexamethasone is required to prevent fluid retention from docetaxel

55
Q

Camptothecins and MOA

A
  • Topotecan, Irinotecan
  • Inhibit Topoisomerase I
  • DNA damage → fragments of single stranded DNA
56
Q

Etoposide MOA

A
  • Inhibits Topoisomerase II (E-two-poside)
  • DNA damage
  • through strand breakage → fragments of double stranded DNA
  • Blocks cell in late S-G2 phase
57
Q

Prednisone

A
  • glucocorticoid
  • lympholytic → suppresses mitosis in lymphocytes
  • Used for acute leukemia and malignant lymphomas, “lymphocyte PRED-ator”
58
Q

Selective Estrogen-Receptor Modulators (SERMs)

Selective Estrogen-Receptor Downregulators (SERDs)

A

SERMs: Tamoxifen, Raloxifene

SERDs: Fulvestrant

59
Q

Tamoxifen vs. Raloxifene

A
  • Tamoxifen:
    • antagonist @ breast
    • agonist @ bone & uterus
    • treatment for receptor-positive breast cancer
    • increased risk of endometrial cancer
  • Raloxifene:
    • antagonist @ breast & uterus
    • agonist @ bone
    • increased risk for thromboembolic events
    • NO increased risk for endometrial cancer
    • Prevention of postmenopausal osteoporosis
    • prophylaxis of breast cancer in high risk postmenopausal women
60
Q

Fulvestrant

A
  • Devoid of all estrogen agonist activity
  • binds to estrogen inhibitor and inhibits dimerization
  • increasing its degradation
  • ER-mediated transcription abolished
61
Q

Aromatase inhibitors (AI)

A

Nonsteroidal reversible competitive inhibitors:
Anastrozole, Letrozole

Steroidal irreversible competitive inhibitors:
Exemestane

62
Q

____ converts androstenedione to estrone

A
  • *Aromatase** converts androstenedione to estrone
  • (primary source of circulating estrogens in postmenopausal women)*

therefore, aromatase inhibitors are standard care of adjacent treatment of postmenopausal women with hormone receptor-positive breast cancer

63
Q

Androgen Inhibitors

A

Gonadotropin-Releasing Hormone Agonists:
Goserelin, Leuprolide
Androgen receptor blockers: Flutamide

64
Q

GnRH Agonists MOA

A
  • Cause initial surge in LH + FSH (1-2 weeks), followed by inhibition of gonadrotropin release
  • testosterone falls to 10% of initial values after 1 month
  • FLUTAMIDE for 2-4 weeks to prevent surge
65
Q
A

Pharmacology (19 decks)

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