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Hem/onc Exam 2 > Pharm: Anti-neoplastic agents > Flashcards

Pharm: Anti-neoplastic agents Flashcards

1
Q

What drug class does Methotrexate (MTX) belong to?

A

Anti-metabolites - a Cell-Specific (CCS) drug

It is a Folic acid analog

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2
Q

What are the 2 main characteristics of Anti-metabolites?

A
  1. Bone marrow cell replication is profoundly inhibited
  2. Highly cell cycle specific: S phase
    (Also: inhibits DNA synthesis, has GI toxicity)
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3
Q

MOA of Methotrexate:

A
  • Inhibits dihydrofolate reductase –> DECREASE IN NUCLEIC ACID SYNTHESIS
  • Binds strongly to DHFR to inhibit formation of MTHF, the folate required for dTMP synthesis
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4
Q

What phase of the cell cycle is the most sensitive to MTX?

A

S-phase

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5
Q

What is the rescue therapy for the toxic effects of MTX?

A

Leucovorin - administered 6-24 hours after MTX administration
-is the METABOLICALLY ACTIVE FORM OF FOLIC ACID

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6
Q

What drug class do Paclitaxel and Docetaxel fit into?

A

Taxanes - Cell Cycle-Specific (CCS) drug

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7
Q

Where does Paclitaxel come from?

A

Bark of the pacific yew

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8
Q

Where does Docetaxel come from?

A

Bark of the English yew

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9
Q

Primary use of Paclitaxel?

A

Solid tumors

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10
Q

MOA of Paclitaxel:

A

BLOCKS A CELL’S ABILITY TO BREAKDOWN THE MITOTIC SPINDLE DURING MITOSIS.
-Thus, CELL CAN’T DIVIDE INTO DAUGHTER CELLS

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11
Q

Paclitaxel route of administration:

A

IV: irritates skin and mucous membranes on contact

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12
Q

Paclitaxel SE:

A

Neurotoxicity

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13
Q

Docetaxel Indications:

A

HORMONE REFRACTORY PROSTATE CANCER (in combo with prednisone.
Also: Breast cancer, non-small cell ung cancer, advanced gastric cancer, squamous cell head and neck cancer

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14
Q

Docetaxel: SE

A

Fluid retention (tx w/ steroids the night before administration of Docetaxel)

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15
Q

Taxanes MOA in general

A

Interfere with mitosis

BIND TO MICROTUBULES and inhibits their depolymerization into tubulin

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16
Q

General SE of Taxanes:

A

Myelosuppression, Hypersensitivity

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17
Q

Vinca alkaloids are important in what drug regimen?

A

MOPP

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18
Q

What are the 3 Vinca alkaloids and their associated SE?

A

Vinblastine, Vinorelbine (Myelosuppression)

Vincristine: Neurotoxicity

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19
Q

What pant do Vinca alkaloids come from?

A

Periwinkle

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20
Q

Vinca alkaloids MOA:

A

BIND TO TUBULIN - thus preventing the cells from making the spindles it needs to be able to move its chormosomes around as it divides
-Colchinine-like ARREST IN METAPHASE

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21
Q

What happens if you inject someone intrathecally with vinca alkaloids?

A

Then done get dead.

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22
Q

Etoposide (VP-16) belongs to what drug class?

A

Epipodophyllotoxins - a cell cycle-specific drug class

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23
Q

General MOA (3 words) of Epipodophyllotoxins:

A

CYTOSTATIC (ANTIMOTOTIC) GLUCOSIDES)

24
Q

What plant do Epipodophyllotoxins come from?

A

EXTRACT OF THE MAYAPPLE

25
Q

What part of the cell cycle do Epipodophyllotoxins target?

A

Cells undergoing mitosis

26
Q

Clinical use of Epipodophyllotoxins:

A

CREAMS SUCH AS CONDYLOX, as well as TOPICAL SOLUTION in treatment for GENITAL WARTS (squamous cell carcinoma

27
Q

What two specific places in the cell cycle does Etoposide act?

A

Blocks the G1 PHASE

Blocks the replication of DNA (S-PHASE)

28
Q

Main clinical use of Etoposide (CP-16):

A

Treat TESTICULAR CANCER which has not responded to other treatments

29
Q

SE of Etoposide:

A

Hypotension, alopecia, n/v, myelosuppression

30
Q

Are Anti-tumor antibodies cell cycle specific or cell cycle non-specific?

A

Cell cycle specific (just less though)

31
Q

Where do antitumor antibodies come from?

A

Streptomyces spp.

32
Q

MOA of Anti-tumor antibodies

A

All Interact with DNA and/or RNA, but may also interact with other cellular substituents.

33
Q

Administration of Anti-tumor antibodies:

A

IV except Bleomycin (IV, IM, SubQ, intrapleural)

34
Q

SE of anti-tumor antibodies:

A

TISSUE NECROSIS

35
Q

MOA of alkylating agents:

A

Form covalent bonds
Intermediates react with nucleophils to form covalent bonds with phosphate, amino, sulhydryl, Carboxy, imidazole groups
CARBONIUM ION INTERACTS WITH NUCLEOPHILIC GROUPS SUCH AS N7 AND O6 OF GUANINE

36
Q

“Timing” target of Alkylating agents:

A

NOT CELL CYCLE SPECIFIC BUT STILLMORE ACTIVE IN DIVIDNG TISSUE

37
Q

Consequences of Alkylating Agents: (2)

A
  • DNA-DNA strand break and DNA-protein cross-link break (Especially by reacting 7-NITROGEN OF GUANINE)
  • Misreading of genetic code: ALKYLATION of guanine may shift electron configuration so it FORMS GT RATHER THAN GC PAIRS
38
Q

What drug class does Cyclophosphamide fit into?

A

Alkylating agents –> Cell cycle Nonspecific (CCNS) drugs

39
Q

MOA of Cyclophosphamide

A

Hepatic Cytochrome P-450 system, enzymes phosphatase and phosphamidase are primarily activators to intermediate ALDOPHOSPHAMIDE (HIGHLY toxic to bladder), which non-enzymatically breaks down to Phosphoramide mustard, Acrolein

40
Q

Effect of Grapefruin on Cyclophosphamide

A

Inhibitor –> CYP 3A4 Inhibitor –> decrease activation of cyclophosphamide

41
Q

Take home from Alkylating Agents?

A

-Directly damages DNA
Have a broad spectrum of ANTI-TUMOR ACTIVY and IMMUNOSUPPRESSION
Cause dose-limiting myelosuppression
-Are genotoxic and associated with an increased risk of leukomogenesis

42
Q

What drug class do Doxorubicin, Daunorubicin, Epirubin, and Idarubicin belong too?

A

Anthracylines –> CCNS drugs

43
Q

MOA Of anthracyclines:

A
  • DNA TOPOISOMERASE II INHIBITORS (DNA replication and transcription
  • INTERCALATES BETWEEN BASE PAIRS OF DNA and inhibits DNA-dependent RNA synthesis
  • GENERATES FREE RADICALS: cause membrane damage and DNA strand breaks
44
Q

Side effects of Anthracyclines:

A
  • Cardiotoxicity (need an ejection fraction of 55% before they can take these drugs)
  • Red discoloration of the urine, Myelosuppression, Amenorrhea, N/V
45
Q

What is special about Doxorubicin?

A

TETRACYCLINE STRUCTURE SUBSTITUED WITH SUGAR (Daunosamine)

46
Q

What drug class do Cisplatin, Carboplatin, and Oxaliplatin belong?

A

Platinum analogs –> CCNS drugs

47
Q

What is the MOA of Cisplatin?

A
  • Enters cell by passive diffusion
  • C1 - MOIETIES REACT WITH N7 OF GUANINE and other nucleophiles
  • Intrastrand (rapidly) and interstrand (slowly) crosslinks in DNA
  • DNA-protein crosslinks
  • Cell-cycle non-specific
48
Q

SE Of Cisplatin:

A

NEPHROTOXICITY

49
Q

Clinical use of Cisplatin:

A

Non-small cell carcinoma

50
Q

Explain Resistance with Cisplatin:

A
  • Inhibition of drug uptake
  • An increase in production of cellular thiols: Metallothionins, Gluathione –> BLOCKS THE FORMATION OF DNA ADDUCTS
  • Changes in the concentration of regulatory proteins
  • An increase in the repair of Cisplatin-DNA
51
Q

What Drug class does Carboplatin belong?

A

Plantinum analogs –> CCNS drugs

52
Q

What is important to know about Carboplatin:

A

Less nephrotoxic than cisplatin

53
Q

1st line treatment in Multiple Myeloma?

A
  • Steroids (dexamethasone) to decrease the inflammation –> symptomatic
  • High dose Chemo + Autologous hematopoietic cell transplant
54
Q

Category 1 tx in Non-transplant patients: (5)

A
  1. Melphalan/Prednisone (MP; Standard)
  2. Melphalan/Prednisone/Bortezemib (MPB)
  3. Melphalan/Prednisone/Thalidonmide (MPT)
  4. Lenalidomide/Low Dose Dexamethasone
  5. Bortezombin/Dexamethasone
55
Q

1st line tx for Hodgkin’s Disease:

A

ABVD –> All given at once

56
Q

2nd Line tx for Hodgkin’s Disease:

57
Q

Tx Of non-Hodgkin’s:

Hem/onc Exam 2 (4 decks)

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