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Pharmacology II - Exam 3 > Chemotherapy Drugs > Flashcards

Chemotherapy Drugs Flashcards

1
Q

What are the two classes of alkylating agent?

A

Nitrogen Mustards
Platinum Analogs

(Also: nitrosoureas and alkylsulfonates, but these weren’t discussed)

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2
Q

MOA of Alkylating Agents?

A

Alkylate DNA at N7 position of guanine…leads to protein miscoding and apoptosis

Can also cause cross-linking of DNA…damaged DNA cannot repair and undergoes apoptosis

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3
Q

Clinical indications of Cyclophosphamide

A 
Lymphomas
Leukemias
Multiple Myeloma
Breast and Ovarian Carcinoma
Small Cell Lung Cancer
Some Autoimmune Conditions
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4
Q

What prevents hemorrhagic cystitis that is a side effect of cyclophosphamide?

A

MESNA: mecaptoethane sulfonate

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5
Q

Clinical Indications of Cisplatin

A

Testicular, Ovarian, Bladder, Non-Small and Small Cell Lung Cancers

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6
Q

Cisplatin has prominent activity during which phase of the cell cycle?

A

S phase

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7
Q

Toxicities of Cisplatin

A
  • Dose-limiting toxicity is cumulateive, leading to irreversible damage to the renal tubules (prevented with mannitol)
  • Ototoxic with tinnitus, hearing loss
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8
Q

Resistance of Alkylating Agents

A
  • Increased DNA repair ability of the tumor cells
  • Decreased transport of alkylating drug into cell
  • Increased production of glutathione and glutathione-associated proteins
  • Increased glutathione S-transferase activity
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9
Q

What are the three subclasses of antimetabolites?

A

Folic Acid Analogs
Purine Analogs
Pyrimidine Analogs

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10
Q

How does Methotrexate work?

A

Folic acid analog that binds to the active site of DHFR

Blocks the formation of THF, resulting in interruption in DNA, RNA, and protein synthesis

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11
Q

Renal excretion of MTX is inhibited when it interacts with…

A

Penicillin
Cephalosporins
NSAIDs

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12
Q

What drug is used in combo with MTX as a rescue drug?

A

Leucovorin: rescues normal cells from toxicity

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13
Q

6-MP and 6-TG are metabolized by ____ to active metabolites ____ and ____

A

HGPRT
TIMP
TGMP

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14
Q

Clinical Uses of 6-MP and 6-TG

A

6-MP: ALL, AML, Crohn’s

6-TG: AML

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15
Q

The purpose of allopurinol with 6-MP use

A

Prevents hyperuricemia by inhibiting 6-MP metabolism by xanthine oxidace

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16
Q

Mechanism of Action of 5-FU

A

5-FU gets converted to 5-FUTP, 5-FdUMP, 5-FdUTP

5-FUMP –> RNA damage
5-FdUMP –> DNA damage and inhibits thymidylate synthase

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17
Q

Uses for 5-FU

A

Colon cancer (5-FdUMP), breast, gastroesophageal, hepatocellular, pancreatic cancer

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18
Q

MOA of vinca alkaloids

A

Binds to B-tubulin and prevents polymerization

Depolymerization of microtubules blocking mitotic spindle formation during M phase

Mitotic arrest at metaphase interferes with chromosome segregation

19
Q

Vinblastine: Indications

A

Hodgkin’s, non-Hodgkin’s
Breast Cancer
Testicular Tumors

20
Q

Vinblastine Toxicity

A

Bone marrow suppression, anorexia, N/V/D, alopecia

21
Q

Vincristine: Indications

A

Childhood Cancer, Childhood Tumors

22
Q

Vincristine: Toxicities

A

Peripheral neuritis/neuropathy with paresthesia, muscle weakness

MARROW SPARING

23
Q

Etoposide, Teniposide: Indications

A

Testicular, Non-small and small cell lung carcinomas, AML, ALL, Hodgkin’s and non-Hodgkin’s

24
Q

Etoposide, Teniposide: MOA

A

Blocks tumor cells in the late S-G2 phase of cell cycle through inhibition of topoisomerase II

25
Q

Topotecan and Irinotecan: Indications

A

Topotecan: Ovarian and small cell lung cancers

Irinotecan: metastatic colon cancer

26
Q

Camptothecins: MOA

A

Inhibit topoisomerase I resulting in DNA strand breakage

27
Q

Doxorubicine: Indications

A

Hodgkin’s and non-Hodgkin’s, breast, ovarian, bladder cancers, ALL

28
Q

Doxorubicin is derived from…

A

Streptomyces

29
Q

Doxorubicine: MOA

A

Intercalation interferes with DNA synthesis

Inhibits topoisomerase II leading to DNA fragmentation

30
Q

Doxorubicine: Toxicities

A

Reversible acute arrhythmias and conduction abnormalities

31
Q

Bleomycin: Toxicities

A

Dose-limiting pulmonary fibrosis that can be fatal

32
Q

Bleomycin: Indications

A

Testicular, squamous cell carcinoma, Hodgkin’s and non-Hodgkin’s

33
Q

Bleomycin: MOA

A

Intercalation, scission, and fragmentation of DNA due to an oxidation reaction mediated by a DNA-bleomycin-Fe complex

34
Q

Cancer Treatment Modalities

A 
Surgery
Radiotherapy
Chemotherapy
Endocrine Therapy
MAB/Biologics
Small Molecule Inhibitors
35
Q

Log-Kill Hypothesis

A

Killing action of CCS (cell-cycle specific) drugs follows first order kinetics (a given dose kills a proportion of a cancer cell population

36
Q

Most solid tumors display what type of pattern?

A

Gompertzian…growth rates decline as tumor expands

37
Q

Dose-limiting toxicity

A

Each cytotoxic drug is associated with a particular organ that effectively limits the max dose of the drug that can be given to a patient

38
Q

Types of Drug Resistance

A
  1. Primary: tumor cells don’t respond to initial chemotherapy
  2. Acquired: develops as a consequence of chemotherapy
39
Q

Examples of Drug Resistance

A
  1. Up-regulation of drug resistance transporters
  2. Down-regulation of methotrexate transporter
  3. Increased expression of DNA repaired enzymes
  4. Increased expression enzymes that produce trapping metabolites within resistant cells
40
Q

CSC Theory to Resistance

A

Anti-cancer treatments can often shrink tumor size by targeting bulk but they fail to target and kill CSCs leading to treatment failure, relapse, and death

41
Q

Properties of CSCs

A

Undergo asymmetric cell division: 1 CSC and 1 daughter cell
Resistant to standard chemotherapy
Resistant to radiation (linked to loss of suppressor gene p53)

42
Q

Principles of Combination Chemotherapy Regimen

A
  1. Drugs with different mechanism of action should be combined
  2. Drugs targeting different populations of cancer cells should be combined CCS with CCNS drugs
  3. Drugs with different organ toxicities should be combined, so full/nearly full therapeutic doses can be utilized for each drug
  4. Drugs associated with different modes of resistance should be combined to minimize cross-resistance
  5. Identify drug combinations that allow for the shortest possible treatment-free period
43
Q

Rapidly growing tumors are most sensitive to…

A

CCS chemotherapeutic drugs

44
Q

CCNS definition

A

Cell Cycle Non-Specific Drugs

Drugs capable of exerting their actions on cancer cells that are cycling or in the resting state

Pharmacology II - Exam 3 (5 decks)

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