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Pharm III > Exam 2 Antineoplastics > Flashcards

Exam 2 Antineoplastics Flashcards

1
Q

Mechlorethamine (Mustargen): class, MOA, SE

A

Antineoplastic: alkylating agent
Part of MOPP regimen; hodgkin
Cause miscoding, breakage and cross-linking
Not cell cycle phase specific
Most effect on rapidly proliferating cells: tumor, GI, hair, bone marrow
SE: vesicant, hematologic, hyperuricemia (tx with alllopurinol), renal damage (must hydrate), N/V, Sterility, teratogenesis
BURN, BLOOD, BARF, BUN, BABY

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2
Q

Alkylating Agent toxicity

A

Vesicant (site injection tissue damage), N/V (CTZ and local), bone marrow depression, immunosuppression, teratogenesis, infertility (incl sperm), alopecia

General: BURN, BLOOD, BARF, BALD, BABY

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3
Q

CYCLOPHOSPHAMIDE (cytoxan): MOA, use, SE

A 
Anti neoplastic Alkylating agent
NOT a vesicant
Broad spectrum
SE: immunosuppressive, alopecia, hematologic toxicity, HEMORRHAGIC CYSTITIS, SIADH
Tx hemorrhagic cystitis with MESNA
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4
Q

List the 3 alkylating agents

A

Mechloerthamine (Mustargen)
Cyclophosphamide (Cytoxan)
Cisplatin (Platinol)

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5
Q

Cisplatin (Platinol): MOA, use, SE

A

Antineoplastic alkylating agent
Crosslinks DNA, sensitizes cells to radiation
Use: Broad spectrum (like Cyclophosphamide)
SE: Nephrotoxic, acoustic n damage, anaphylaxis

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6
Q

List the anti-metabolite agents

A
  1. Methotrexate
  2. Mercaptopurine (6MP, purinethol)
  3. 5-FU (adrucil)
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7
Q

Methotrexate: Class, MOA, how to decrease toxicity? Resistance, use?

A

Antineoplastic antimetabolite
Inhibits DHF reductase, no thymidylate
Blocks DNA, RNA and protein synthesis
Decrease toxicity with Leucovorin (bypass blockade)
Resistance: decrease uptake/increase amt enzyme
Wide use

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8
Q

How is Methotrexate toxic

A
  1. Precipitates in renal tubules – need to hydrate
  2. Hepatotoxic – esp with long term use (ie immunosuppressant for RA)
  3. Myelosuppression
  4. Alopecia
  5. GI
  6. Pulmonary
  7. Teratogenic, sterility
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9
Q

Purine Analogues: class, use, MOA

A 
Antimetabolic antineoplastics
Converted by HGPRT to nucleotide; inhibit synthesis of purine nucleotides (aka DNA, RNA)
Resistance with decreased HGPRT
Not cell cycle specific
Myelosuppressive
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10
Q

6-MP: class, SE, metabolism

A

Antimetabolite antineoplastic
Purine analogue
Metab by xanthine oxidase
May cause hyperuricemia (tx with allopurinol, but will need to decrease 6MP dose)
Toxicity: Bone marrow depression, jaundice

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11
Q

5-FU class, MOA, use

A

Antimetabolite antineoplastic agent
Inhibits thymidylate synthase and thus blocks DNA synthesis (specific to G1 and S phase)
Response increased by leucovorin (FH4 needed to form thymidylate synthase complex
Broad use, topical BCC

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12
Q

Doxorubicin (adriamycin) class, MOA, use

A

Antibiotic antineoplastic
Intercalates/STICKS into DNA, generates free radicals, effect increased by iron
Cardiotoxic esp with herceptin
Wide use
Daunorubicin makes urine turn red/orange but less cardiotoxicity

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13
Q

Bleomycin (Blenoxane) class, MOA, efficacy, SE

A

Antibiotic Antineoplastic
Directly damages DNA
G2, M phase specific
Oral or into bladder
Highly Effective – testicular, ovarian
SE: little bone marrow depression, pulmonary fibrosis, anaphylactoid sx
*lance Armstrong wouldn’t take Bleo bc risk pulmonary fibrosis – BleNOXane – NO Oxygen

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14
Q

What are the various mechanisms of CA chemo

A
  1. Alkylate DNA
  2. Interfere with metab (antimetabolites)
  3. Bind to microtubules
  4. Block hormones
  5. Antibodies
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15
Q

Strategies for treating cancer include

A
  1. Destroy CA cells
  2. Remove CA (surgery)
  3. Prevent mets
  4. Convert tumor to normal cell
  5. Halt neoplastic cell division
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16
Q

What determines the likelihood of CA tx success?

A

Better if…

a) fast growing tumor
b) high % of cells in growth fraction
c) small tumors
d) early detection (less invasive, no mets)

17
Q

How do CA cells becomes resistant to drugs

A

Changes in level/affinity of target enzymes
Decreased drug activation
Increased DNA repair
Increased salvage pathways for purines and pyrimidines
Decreased drug uptake
Increased drug efflux

18
Q

Where does tx toxicity occur

A

Rapidly growing cells

a) bone marrow (common; may lead to increased bleeding after other procedures)
b) GI tract: N/V, irritation
c) Hair follicles: alopecia
d) Renal: nephrotoxicity
e) Reproduction: infertility and teratogenesis

19
Q

Nitrogen mustard used to…

A

Treat lymphoma

20
Q

Plant Alkaloids include

A

Vinblastine, Vincristine, Paclitaxel (Taxol)

21
Q

Plant Alkaloids: MOA, use

A

Bind to tubulin, disrupt mitosis, prevent segregation of chromosomes lined up (Vinblastine and Vincristine block polymerization)
Cell cycle specific – M PHASE

Resistance due to increase P glycoprotein

22
Q

Vincristine/Vinblastine class, MOA, SE

A

Plant alkaloid antineoplastic agent
Bind to tubulin M phase
Axonal transport also uses microtubules
*Vincristine: crisps the neurons, low myelosuppression
*Vinblastine: blasts the bone marrow, less neurotoxicity

23
Q

Paclitaxel (Taxol) class MOA, use

A

Plant alkaloid antineoplastic agent
binds tubulin/microtubuline, arrests mitosis, disrupts axonal transport
Kaposis sarcoma
SE: myelosuppression, myalgias, peripheral neuropathy, hypersensitivity
Tax is toxic to tubulin

24
Q

Imatinib (Gleevec) class, MOA, use, SE

A

Tyrosine Kinase inhibitor antineoplastic
inhibits Bcr-Abl fusion protein (tx for CML)
SE: NVD, edema, myalgia, can be immunosuppressive
No immunizations, avoid if recently immunized for polio

25
Q

Cetuximab class, moa

A

Epidermal growth factor inhibitor (EGF Receptor) antineoplastic

26
Q

Erlotinib class, MOA, SE

A

EGF inhibitor antineoplastic
Blocks ATP binding to HER1/EGFR tyrosine kinase
SE: diarrhea, rash, anorexia, fatigue

27
Q

Summarize hormones and antagonist and breast CA drugs

A

Prednisone: lymphoma and leukemia (MOPP)

Tamoxifen: block estrogen R in breast (SE: hot flash, uterine hyperplasia)

Tastuzumab (Herceptin): antibody to HER2 R (SE: cardiac toxicity esp with doxorubicin)

Flutamide: anti-androgen for prostate CA

28
Q

Bevacizumab (Avastin) MOA, use, SE

A

Angiogenesis VEGF Inhibitor: antineoplastic
VEGF (vascular endothelial growth factor) is needed for angiogenesis, but overexpressed in tumors
Decreases Blood supply and slows tumor growth
Injected in eye for macular degeneration RANIBIZUMAB
Risks: bleeding and thromboembolism
Sunitinib (renal CA) and Sorafenib (HCC) very similar, SE similar

29
Q

Sunitinib, Sorafenib

A

Similar to Bevacizumab (angiogenesis VEGF inhibitor)
decreases blood supply, slows tumor growth
Sunitinib: renal CA
Sorafenib: HCC

Pharm III (9 decks)

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