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Heme Test 2 > Antineoplastic Agents > Flashcards

Antineoplastic Agents Flashcards

1
Q

cyclophosphamide

A

alkylating agent, CCNS

AE: Allopecia and hemorrhagic cystitis, prevented through *Mesna

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2
Q

Ifosfamide

A

alkylating agent, CCNS

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3
Q

busulfan

A

alkyl sulfonate, CCNS

AE: pulmonary fibrosis, hyperpigmentation

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4
Q

cisplatin

A

platinum coordination complex, CCNS

AE’s: renal tubular damage, ototoxicity, Vomiting

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5
Q

methotrexate

A

aka “MTX”

antimetabolite, CCS S phase

  • Inhibits dihydrofolate reductase (DHFR): inhibits conversion of folic acid to tetrahydrolic acid

Indications:
Cancer
Rheumatoid arthritis
Psoriasis

Rescue drug = *Leucovorin

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6
Q

fluorouracil

A

aka “5-fluorouracil; 5-FU”

pyrimidine analog: CCS S-phase

MOA:

  • inhibits DNA synthesis
  • Active compound (FdUMP) covalently binds thymidylate synthetase and blocks de novo synthesis of thymidylate
  • Active compounds (FdUTP and FUTP) are incorporated into both DNA and RNA, respectively
  • *Leucovorin can’t rescue
  • use: colorectal cancer
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7
Q

mercaptopurine

A

aka “6-mercaptopurine; 6-MP”

purine analog: CCS S-phase

MOA:

  • Inhibition of several enzymes of de novo purine nucleotide synthesis
  • Incorporates into DNA and RNA

NOTE: interaction with allopurinol

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8
Q

vinblastine

A

vinca alkaloid: CCS M phase

AE’s: alopecia, myelosupression, neurotoxicity (numbness and tingling of the extremities, loss of deep tendon reflexes, motor weakness, autonomic dysfunction has also been observed)

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9
Q

vincristine

A

vinca alkaloid: CCS M phase

AE’s: alopecia, myelosupression (less than vinblastine), neurotoxicity (numbness and tingling of the extremities, loss of deep tendon reflexes, motor weakness, autonomic dysfunction has also been observed)

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10
Q

paclitaxel

A

taxanes: CCS M phase

AE’s: Hypersensitivity reactions in hands and toes, change in taste

Indicated for treatment of several solid tumors

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11
Q

etoposide

A

epipodophyllotoxin - CCS S-G2 phase

inhibits Type II Topoisomerases, which cut both strands of double-stranded DNA simultaneously to wind and unwind DNA supercoils (CCS - S, G1, G2 phases)

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12
Q

doxorubicin

A

antibiotic: CCNS

MOA:

  1. inhibits Type II Topoisomerases, which cut both strands of double-stranded DNA simultaneously to wind and unwind DNA supercoils (CCS - S, G1, G2 phases)
  2. intercalate DNA
  3. Oxygen free radicals bind to DNA causing single- and double-strand DNA breaks

AE: Free radicals are linked to significant cardiotoxicity
Cumulative cardiac damage can lead to dysrhythmias and heart failure

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13
Q

bleomycin

A

antibiotic anthracenedione: CCS: G2-M phase

MOA: MOA: Free radicals cause single- and double-strand DNA breaks
- Cell cycle specific (G2 arrest)

AE: pulmonary toxicity (5-10%, usually presents as pneumonitis with cough, dyspnea, dry inspiratory crackles)

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14
Q

L-Asparaginase

A

enzyme
CCS - G1 phase

MOA: hydrolyzes circulating L-asparagine into aspartic acid and ammonia, effectively inhibiting protein synthesis

Adverse Effects:

  • Acute hypersensitivity reaction
  • Delayed toxicities include an increased risk of clotting and bleeding, pancreatitis, and CNS toxicity including lethargy, confusion, hallucinations, and coma

indication: targeted for ALL - ALL tumor cells lack the enzyme asparagine synthetase and thus require an exogenous source of L-asparagine

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15
Q

Imatinib

A

protein tyrosine kinase inhibitor: BCR-ABL

The BCR-ABL fusion protein results from the t(9:22) translocation and is found in 95% of patients with CML

Imatinib is a small molecule inhibitor of the ABL tyrosine kinase and has been hailed as a conceptual breakthrough in targeted chemotherapy

Imatinib can also inhibit the RTKs PDGFR and c-KIT

  • see interactions with other drugs that induce the CYP450 system*
  • assoc/ w/ less toxicity than others due to only inhibiting protein tyrosine kinases that are only seen on cancer cells - don’t have as much myelosuppression
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16
Q

Trastuzumab

A

monoclonal antibodies - antigen to tyrosine kinase

** breast cancer tx **

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17
Q

Leucovorin

A

rescue agent - Used to rescue normal cells from high-dose MTX (allows normal cells to continue DNA synthesis)

  • reduced folate can bypass DHFR
  • Antidote for accidental MTX overdose
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18
Q

Mesna

A

rescue agent - prevents hemorrhagic cystitis (attack of bladder lining) - that is associated with cyclophosphamide

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19
Q

Filgrastim

A

G-CSF

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20
Q

Erythropoietin

A

anemia

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21
Q

Ondansetron

A

anti-emesis, serotonin antagonist

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22
Q

-platin

A

platinum coodination complex - alkalating agents

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23
Q

Vin-

A

Vinca alkaloids

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24
Q
  • taxel
A

taxanes

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25
-poside
epipodophyllotoxins
26
-tecan
camtothecins
27
-inib
protein tyrosine kinase inhibitor
28
-zumab
monoclonal antibodies
29
CCS?
``` antimetabolits - S phase etoposide = S-G2 phase Bleomycin = G2-M phase Taxanes = M phase Vinca alkaloids = M phase Camptothecins = S phase ```
30
CCNS?
Alkalating agents Antimetabolites Antitumor antibiotics Platinum analogs
31
Growth fraction
= the ratio of proliferating cells to resting cells (G0) Growth fraction is a determinant of responsiveness to chemotherapy The initial growth rate of most solid tumors is rapid but decreases over time ``` Cells with high growth fraction: Bone marrow GI tract Hair follicles Sperm-forming cells ``` high growth fraction = shorter doubling time (CCS drug) low growth fraction = longer doubling time (should use CCNS) Burkitt lymphoma (high growth fraction; curable by chemotherapy) vs. colorectal carcinoma (low growth fraction; chemotherapy has minor activity)
32
MDR1 gene
ATP-dependent transporter gene amplification in neoplasms confers resistance to a broad range of agents used in cancer treatments The P-glycoprotein is an ATP-dependent efflux pump that actively pumps antineoplastic agents out of cells (MDR1 gene) Anthracyclines, vinca alkaloids, etoposide, paclitaxel, and dactinomycin
33
MOA of alkalating agents?
form covalent linkages with DNA --> resulting in intrastrand linking and interstrand linking and cross-linking --> prevents unwinding of DNA, results in shut-down of replication process
34
alkylating agent toxicity?
Direct vesicant effects and tissue damage at site of injection (oral administration is of great clinical benefit) Many alkylating agents produce acute toxicity, such as nausea and vomiting within 30-60 minutes (pretreat with serotonin antagonist) Delayed toxicities include the common side effects of antineoplastics: bone marrow depression with leukopenia, thrombocytopenia, nephrotoxicity, alopecia, mucosal ulceration, intestinal denudation
35
MOA of antimebolites?
- Structural analogs to compounds necessary for cell proliferation - Block or subvert pathways that are involved in, or lead to, cell replication (nucleotide and nucleic acid synthesis) **Cell cycle specific (S phase) 1. Folic acid analogs (methotrexate) 2. Pyrimidine analogs (5-Fluorouracil) 3. Purine analogs (6-mercaptopurine)
36
allopurinol interactions?
Biotransformation of 6-MP includes metabolism to the inactive metabolite 6-thiouric acid by xanthine oxidase (first pass effect in liver) Allopurinol, a xanthine oxidase inhibitor, is often used as supportive care in the treatment of acute leukemias to prevent hyperuricemia due to tumor cell lysis Simultaneous administration of allopurinol and oral 6-MP results in increased levels of 6-MP and increased toxicity Reduce oral 6-MP dose by 50-75%; IV dose unaffected
37
AE's of antimetabolites?
Relatively little acute toxicity after an initial dose Common toxicities include diarrhea, myelosuppression, nausea, vomiting, immunosuppression, thrombocytopenia, leukopenia, hepatotoxicity
38
MOA of Vinca Alkaloids?
Bind to β-tubulin and inhibit microtubule assembly Cell cycle specific mitosis inhibition (M-phase) ex: vinblastine, vincristine
39
MOA of Taxanes?
- Bind to β-tubulin and stabilize microtubule assembly - Cell cycle specific mitosis inhibition (M-phase) ex: paclitaxel
40
pulmonary toxicity?
bleomycin, busulfan
41
Erlotinib and Gefitinib
MOA: Inhibit Epidermal Growth Factor Receptor (EGFR), a receptor tyrosine kinase **Preferred single-agent first-line therapy for NSCLC patients with somatic activating EGFR mutations AE: Produce dermatologic toxicities
42
tyrosine kinases action?
When mutated, overexpressed, or structurally altered, tyrosine kinases can become potent oncoproteins Abnormal activation of tyrosine kinases has been found in many human neoplasms Aberrant tyrosine kinase activity can occur in receptor tyrosine kinases or cytoplasmic kinases --> promoting survival, proliferation and growth Intracellular (nibs) vs. extracellular (mabs)
43
ototoxicity?
Cisplatin
44
Mucositis?
methotrexate, melphalan
45
Cardiotoxicity?
doxorubicin, daunorubicin
46
peripheral neuropathy?
vincristine
47
pulmonary fibrosis?
bleomycin, busulfan
48
nephrotoxicity?
cisplatin, cyclophsophamide
49
hemorrhagic cystitis?
cyclophsophamide, ifosfamide
50
12 y/o male evaluated in hematology clinic b/c of fatigue and peripheral blood eos, presents with intermittent cramping, pain in arms and legs and anterior c/p thats worse with mvmt, deep breathing, coughing - HR is 120, palpable lymph nodes in inguinal regions - bippsy shows marked hypercellular with eos and erythroid elements, amid clusters of blasts with irregular nuclei. blood smear shows leukocytosis with marked eos. Cytogenetic FISH analysis shows t(15;14) - pt. ddx with ALL . cell cycle specific manner?
antimetabolites: mercaptopurine, methotrexate, fluorouracil
51
which agent is administered with high dose MTX to rescue healthy cells?
leucovorin - bypasses dihydrofolate reductase (enzyme inhibited by MTX) in the cycle and enters in later, results in production of nucleotide precursors in normal cells
52
66 y/o female with CBC drawn during her annual physical shows WBC count of 60,000 and 90% neutrophils, hematocrit of 32%, platelet count of 300,0000. only pertinent PE is splenomegally. Has AML... with t(9;22), phildadelphia chromosome, BCR-ABL. which drug to use? assuming mutation has occurred in BCR-ABL fusion protein, which agent is best to use?
BCR-ABL results in unregulated tyrosin kinase activity, implictated in malignant transformation due to effects on cell cycle, inhibition of apoptosis and increased proliferation of cells - 1. use Imatinib - a protein tyrosine kinase inhibitor which inhibits BCR-ABL kinase 2. Dasatinib - it inhibits BCR-ABL also used when there is resistance to Imatinib
53
Her2/neu positive?
trastuzumab - monoclonal antibodies continued cancer growth after remission would be due to? drug resistance
54
deferoxamine?
antidote for iron poisoning
55
N-acetylcsteine?
antidote for tyelonl
56
Vit K?
antidote for coumadin/warfarin
57
CCNS? acts by intercalating into DNA strands?
doxorubicin (doesn't actually bind to the DNA, not a covalent bond) alkylating agents (include cyclophosphamide and ifossfamide) form COVALENT bonds with the DNA however BOTH prohibit DNA from unwinding and are CCNS
58
mechlorethamine?
alkylating agent - it alkylates DNA, causing cross-links b/w parallel DNA strands
59
most likely condition for which methotrexate is given other than cancer?
rheumatoid arthritis
60
antimetabolites?
CCS- inhibit S phase 5-Fluorouracil 6-Mercaptopurine Methotrexate
61
epipodophyllotoxins?
CCS: S-G2 phase through inhibiting topoisomerase II *natural product ex. Etoposide
62
Antitumor antibiotics?
CCS: G2-M phase * natural product ex. Bleomycin
63
Taxanes?
Mphase: stabilze MT's by binding to Beta tubulin ex. Paclitaxel
64
Vinca Alkaloids?
Natural product M phase, by inhibiting microtubule assembly ex. Vinblastine, vincristine
65
Alkylating agents?
CCNS ex. Cyclophosphamide, Ifosfamide, Busulfan, Cisplatin
66
Anthracyclines?
CCNS, in the natural class of antibiotics ex. Doxorubicin
67
tx of CML with, BCR-ABL
Imatinib
68
NSCLC?
Gefitinib, erlotinib
69
treatment of CML resistant to imatinib
Dasatinib
70
HER2/Neu
Trastuzumab
71
Which of the following effects are anticipated in response to imatinib therapy
Interactions with other drugs that induce the CYP450 system
72
Rituximab
CD20, Non-Hodkins lymphoma
73
Alemtuzumab
CD52, chronic lymphocytic luekemia
74
Gemtuzumab
CD33, AML
75
Cetuximab
EGFR (ErbB-1) | colorectal, lung, pancreatic, breast
76
Bevacizumab
VEGF, Colorectal cancer, lung
77
trastuzumab?
watch out for cardiac toxicity
78
Ibratumomab/Tositumomab
CD20, NLH
79
CD20, nonhodkins lymphoma
use rituximab OR Ibritumomab, Tositumomab
80
which causes problems with CNS?
Asparaginase and Cytarabine
81
CD52
chronic lymphocytic leukemia, Alemtuzumab
82
CD33
AML, Gemtuzumab
83
EGFR (ERB-1)
Colorectal, lung, pancreatic, breast cancer - Ceftuximab
84
VEGF
Colorectal, lung cancer | - Bevacizumab

Heme Test 2 (4 decks)

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