Pharmacology > Anticancer > Flashcards

Anticancer Flashcards

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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
6-MP and 6-TG AEs
* Nausea, vomiting, diarrhea * bone marrow suppression, * hepatotoxicity (6-MP)
26
6-thioguanine (6-TG) MOA
converted to nucleotide → inhibits purine synthesis and phosphorylation of GMP to GDP, can be incorporated into RNA and DNA
27
5-FU inhibits ___ resulting in \_\_\_\_.
5-FU inhibits **thymidylate synthase** resulting in **'thymineless death'.**
28
Combination chemotherapy used for colorectal cancer
**5-FU and LEUCOVORIN** *Leucovorin increases N5,N10-methylene-THF, potentiating 5-FU (which inhibits thymidylate synthase)*
29
5-FU and Capecitabine AEs
* **HAND-FOOT SYNDROME:** erythematous desquamation of the palms and soles seen after extended infusions
30
Cytarabine (ARA-C) MOA
*(deoxycytidine analog)* phosphorylated to triphosphate → incorporated into DNA → **inhibits DNA polymerase** *"tara takes double penetration"*
31
Antitumour Antibiotics MOA
* 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
Doxorubicin & Daunorubicin MOA
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
\_\_\_ is an iron-chelating agent educing cardiotoxicity from \_\_\_\_
**Dexrazoxane** is an iron-chelating agent educing cardiotoxicity from **Doxorubicin**
34
Bleomycin cell specific phase it acts on
**G2 phase**
35
Alkylating Agents MOA
* 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
Alkylating Agents AEs
* **MUTAGENIC + CARCINOGENIC** * particularly in rapidly growing tissues
37
list the Nitrogen Mustards
mechlorethamine, cyclophosphamide, melphalan ("MCM = Mel Phalan")
38
\_\_\_\_ is a metabolite of cyclophosphamide, responsible for \_\_\_\_\_.
**Acrolein** is a metabolite of cyclophosphamide, responsible for **hemorrhagic cystitis**.
39
list ways of preventing hemorrhagic cystitis
* adequate fluid intake * mesna * acrolein
40
list Nitrosoureas and its properties
* Carmustine, Lomustine * very lipophilic, can cross BBB * useful treatment for **BRAIN tumours**
41
Busulfan toxicity
Pulmonary fibrosis, myelosuppression
42
\_\_\_\_ is converted by liver P450 enzymes to alkylating metabolites
**Procarbazine** is converted by liver P450 enzymes to alkylating metabolites
43
Procarbazine AEs
* 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
Cisplatin, Carboplatin MOA treatment for which cancers?
* 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
Cisplatin AEs
* **Nephrotoxicity, ototoxicity** * **Peripheral neuropathy** * Mild/Moderate Myelosuppresion
46
Carboplatin AEs
* less nausea, neurotoxicity, ototoxicity, nephrotoxicity than cisplatin * dose-limiting toxicity is myelosuppression
47
Vinca alkaloids/mictotubule inhibitors
Vicristine, vinblastine
48
Vicristine, vinblastine (Vinca alkaloids) MOA
* bind to B-tubulin and **inhibits** **polymerization** of microtubules * Arrest in **M phase** * Cell division stops → apoptosis
49
Vinca Alkaloids AE
* Vincristine: **peripheral neuropathy** * Vinblastine: **dose-limiting myelosuppresion**
50
list the taxanes and their MOA
* Paclitaxel, Docetaxel * Bind to B-tubulin of microtubules and **promote microtubule polymerization** * stabilization of microtubules arrests cells in **mitosis** → apoptosis
51
Paclitaxel AEs
* Hypersensitivity * peripheral neuropathy
52
Hypersensitivity from Paclitaxel is reduced by premedication with...
Dexamethason, Diphenydramine, H2 blocker
53
Docetaxel Adverse Effects
* **fluid retention** * peripheral neuropathy (not as frequently as paclitaxel) * Myelosuppression is dose-limiting
54
pretreatment with ____ is required to prevent fluid retention from docetaxel
pretreatment with **Dexamethasone** is required to prevent fluid retention from docetaxel
55
Camptothecins and MOA
* **Topotecan, Irinotecan** * Inhibit Topoisomerase I * DNA damage → fragments of single stranded DNA
56
Etoposide MOA
* Inhibits Topoisomerase **II** (E-two-poside) * DNA damage * through strand breakage → fragments of double stranded DNA * Blocks cell in **late S-G2 phase**
57
Prednisone
* glucocorticoid * lympholytic → suppresses **mitosis** in **lymphocytes** * Used for acute leukemia and malignant lymphomas, "lymphocyte PRED-ator"
58
Selective Estrogen-Receptor Modulators (SERMs) Selective Estrogen-Receptor Downregulators (SERDs)
SERMs: Tamoxifen, Raloxifene SERDs: Fulvestrant
59
Tamoxifen vs. Raloxifene
* 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
Fulvestrant
* **Devoid** of all estrogen **agonist** activity * binds to estrogen inhibitor and inhibits dimerization * increasing its degradation * ER-mediated transcription abolished
61
Aromatase inhibitors (AI)
Nonsteroidal reversible competitive inhibitors: **Anastrozole, Letrozole** Steroidal irreversible competitive inhibitors: **Exemestane**
62
\_\_\_\_ converts androstenedione to estrone
* *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
Androgen Inhibitors
Gonadotropin-Releasing Hormone Agonists: **Goserelin, Leuprolide** Androgen receptor blockers: **Flutamide**
64
GnRH Agonists MOA
* 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
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