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IHO 4 > Antineoplastics IV > Flashcards

Antineoplastics IV Flashcards

1
Q

Vinca alkaloids

A

Vinblastine, vincristine, vinorelbine

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2
Q

Taxanes

A

Paclitaxel (cabazitaxel, docetaxel)

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3
Q

Epilone

A

Ixabepilone

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4
Q

Vinca alkaloids MOA

A

-Bind tubulin at forming end of microtubules and TERMINATE spindle assembly

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5
Q

Vinca alkaloids resistance

A
  • decreased accumulation via increased P-glycoprotein expression –>MDR
  • Changes in target proteins (mutations in tubulin).
  • Cross reactivity among vinca alkaloids not absolute
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6
Q

Vincristine therapeutic uses

A

MOPP for Hodgkin’s disease

CHOP for non-Hodgkin’s lymphoma

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7
Q

Vinblastine therapeutic uses

A

ABVD for Hodgkin’s disease.

PVB for testicular cancer.

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8
Q

Vinca alkaloid toxicity

A

-Bone marrow suppression
-Neurotoxicity
(Vincristine has more CNS toxicity–fatal if given intrathecally) (Vinblastine more bone marrow suppression)
-Nausea and vomiting (greater for vinblastine)
-Vesicant
-Alopecia

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9
Q

What is used as an indication of sufficicent dose of vinca alkaloids?

A

Depression of deep tendon reflexes within 2-3 weeks in 100% of patients

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10
Q

What is an indication to decrease dose of vinca alkaloids?

A

Severe paresthesias and mild to moderate sensory loss

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11
Q

Taxane MOA

A

Binds to tubulin to ENHANCE AND STABILIZE spindle assembly

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12
Q

Taxane resistance

A

Decreased accumulation via increased P-glycoprotein expression –> MDR

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13
Q

Taxane pharmacokinetics

A

Extensive CYP450 metabolism

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14
Q

Taxane toxicity

A
  • Bone marrow suppression
  • Hypersensitivity/allergic reactions
  • Peripheral neuropathy
  • Nausea and vomiting
  • Hypotension, arrhythmias
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15
Q

What form of paclitaxel has reduced toxicity

A

albumin-bound

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16
Q

Epilone (Ixabepilone)MOA

A

Binds tubulin to ENHANCE AND STABILIZE spindle assembly.

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17
Q

Ixabepilone used with capecitabine for 3rd line treament of what? Why 3rd line?

A

Breast cancer. Used in patients who have failed anthracycline antibiotic and taxane treatments (Ixabepilone doesn’t cause MDR resistance)

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18
Q

Where is ixabepilone metabolized?

A

Liver

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19
Q

Ixabepilone toxicity

A
  • Bone marrow suppression
  • Peripheral neuropathy
  • Cardiac arrhythmias
  • Hypersensitivity
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20
Q

Glucocorticoids

A

Dexamethasone and prednisone

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21
Q

Antibiotics

A

Cyclosporine and tacrolimus

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22
Q

mTOR inhibitors (also antibiotics)

A

Everlolimus, temsirolimus

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23
Q

Antibodies and fusion proteins

A

Alemtuzumab, denileukin diftitux, ibritumomab, rituximab, tositumomab

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24
Q

Glucocorticoids MOA

A
  • Interfere with concentration, distribution and function of leukocytes (increase neutrophils, decrease T and B lymphocytes, monocytes etc.)
  • Causes decrease in cytokine release *including decrease in IL-2 and TNF-alpha
  • Decrease size of lymph nodes and spleen
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25
Q

Antibiotics used to prevent rejection following bone marow transplants

A

Cyclosporine and tacrolimus

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26
Q

Angiogenesis inhibitors

A

Everolimus and temsirolimus

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27
Q

Immunosuppressive antibiotic functions

A
  • NFAT mediated regulation of IL synthesis

- mTOR regulation of cell growth and angiogenesis

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28
Q

Immunosuppressive antibiotic MOA

A
  • interfere with intracellular processes that are key for cell proliferation and cytokine production and release.
  • interfere with one of two intracellular signaling cascades
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29
Q

Immunosuppressive antibiotic MOA pathway 1

A

Antirejection

-Bind to cytoplasmic proteins and inhibit calcineurin

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30
Q

Calcineurin

A

needed for activation of NFAT to decrease release of IL-2 and decreased cell proliferation

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31
Q

Cyclosporine binds what?

A

Cyclophilin

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32
Q

Tacrolimus binds what?

A

FK-binding protein

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33
Q

Immunosuppressive antibiotic MOA pathway 2

A

Anti-angiogenesis and anti-proliferation

-Everolimus and temsirolimus function as mTOR inhibitors

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34
Q

Drugs that target CD20

A
  • Rituximab
  • Ibritumomab
  • Tositumomab
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35
Q

CD20 drug target use

A

B-cell non-hodgkin’s lymphoma

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36
Q

Drug that targets CD52

A

Alemtuzumab

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37
Q

CD52 drug target use

A

B cell chronic lympocytic leukemia

38
Q

Denileukin diftitux

A
  • fusion protein that has diphtheria toxin coupled to Il-2
  • goal to kill cells expressing IL-2 receptors
  • Approved for use in cutaneous T-cell lymphoma
39
Q

What does the diphtheria toxin do?

A

Catalyzes ADP-ribosylation of elongation factor-2–> inhibits protein translation by inactivating EF2

40
Q

Antibodies and fusion protein resistance

A

-Changes in target protein that prevent Ab from recognizing antigen

41
Q

Antibodies and fusion protein pharmacokinetics

A

IV admin

long half lives

42
Q

Antibodies and fusion protein toxicity

A 
Infusion reactions (common)
Hypersensitivity reactions (fever, muscle aches, headache, rashes, anaphylaxis)
Infections
43
Q

Specific toxicities for anti-CD Ab

A
  • cardiac arrhythmias
  • tumor lysis syndrome
  • Alemtuzumab: cough, tightness in chest, suspicion that radiolabelled ab (ibritumomoab, tositumomab) may be more likely to cause birth defects
44
Q

Cytokines

A

IFN-alpha
IL-2
TNF-A

45
Q

IL-2 general characteristics

A
  • not directly cytotoxic (induces and expands T cell response cytolytic for tumor cells)
  • used alone or with adoptive cellular therapy
  • short half-life (continuously infused or multiple daily doses)
46
Q

IL-2 side effects

A

Cytokine storm–activating a ton of cascades.
Fever/chills, diarrhea, weight gain, hand foot syndrome.
Can cause shock, thrombocytopenia, respiratory distress, FATAL HYPOTENSION

47
Q

IFN-A MOA (3)

A
  1. Decreases fibroblast growth factor (FGF) production
  2. Inhibtion of cell division of both normal and tumor cells.
  3. Increases MHC-I expression on tumor cells
48
Q

IFN-A side effects

A
  • flu-like symptoms
  • hypotension
  • myelosuppression
  • DEPRESSION
49
Q

TNF-alpha general info

A
  • Cause fibroblast proliferation, chemokine induction, T and B cell activation.
  • Effects on many cell types
  • INTRA-ARTERIAL ADMIN due to extremely short half-life!
  • MALAISE AND FLU-LIKE SYMPTOMS that can cause HEMORRHAGIC NECROSIS
50
Q

Hematopoietic agents

A

erythropoietin (RBC) , filgrastim (G-CSF), IL-11 (platelets), romiplostim, sargramostim (GM-CSF)

51
Q

Drugs that target protein function

A
  • Tyrosine kinase inhibitors

- Drugs targeting altered intracellular processes

52
Q

Bcr-Abl tyrosine kinase inhibitors and the cancer type they treat

A

BOSUTINIB, DASATINIB, IMATINIB, NILOTINIB

-Chronic myeloid leukemia (CML)

53
Q

EGFR tyrosine kinase inhibitors and cancer types they treat

A

CETUXIMAB, ERLOTINIB, GEFITINIB, PANITUMUMAB

-Epithelially derived cancer

54
Q

HER2 tyrosine kinase inhibitors and cancer type that they treat

A

PERTUZUMAB, TRASTUZUMAB [ADO-TRASTUZUMAB EMTANSINE]

-Breast cancer

55
Q

PDGF-R and VEGF-R tyrosine kinase inhibitors

A

PAZOPANIB, SORAFENIB, SUNITINIB

56
Q

tyrosine kinase

A
  • regulators of intracellular signal transduction pathways responsible for development of multicellular communication
  • phosphorylate tyrosine residues
57
Q

Signal transduction inhibitor ending

58
Q

c-kit tyrosine kinase inhibitor and cancer type they treat

A

DASATANIB, IMATINIB, NILOTINIB, SUNITINIB,

-GIST

59
Q

Inhibitors of EGFR (Cetuximab and panitumumab) MOA

A

Prevent actions of EGFR and identify cells expressing the receptor as foreign (targets of cell mediated immunity)

60
Q

Side effects of Cetuximab and Panitumumbab

A
  • infusion, hypersensitivity reactions
  • Infections
  • Rash, photosensitivity, lung (interstitial lung disease)
61
Q

Trastuzumab MOA

A

-Binds Ab and interferes with HER2 singnaling, identifying cells as foreign so they can be destroyed by the immune system

62
Q

Pertuzumab MOA

A
  • DIMERIZATION INHIBITOR

- prevents HER2 from dimerizing with other HER receptors

63
Q

Ado-trastuzumab emtansine MOA

A

-Internalized and undergoes lysosomal degradation to form 2 component (trastuzumab and DM1)

64
Q

DM1 function

A

small molecule inhibitor that disrupts microtubule networks by binding to tubulin

65
Q

Resistance to HER2 inhibitors

A

Altering HER2 so that Ab doesn’t recognize its target

66
Q

Trastuzumab side effects

A
  • Infusion/hypersensitivity reactions
  • Infections
  • Birth defects/fetal loss
  • VENTRICULAR DYSFUNCTION and CHF
67
Q

Drugs that target altered intracellular processes general concepts

A
  • Less selective

- Greater # of side effects

68
Q

Drug that depletes asparagine

A

L-asparaginase

69
Q

L-asparaginase MOA

A

Deprives tumor cells of asparagine and causes selective toxicity

70
Q

L-asparaginase side effects

A

Hypersensitivity reactions

71
Q

Caveats when using L-asparaginase in combination

A
  • Sequence of drug admin is critical!!!
  • MTX given first, have synergistic cytotoxicity (higher cell kill)
  • if L-asparaginase first, see reduction in toxicity (MTX depends on the enzymes needed for being DNA synthesis)
72
Q

Drugs that inhibit proteosome

A

Bortezomib (reversible) and carfilzomib (irreversible)

73
Q

MOA of drugs that inhibit proteosome (bortezomib and carfilzomib)

A
  • Inhibitors of 26S proteasome (complex that degrades ubiquitinated proteins)
  • Inhibitons affects multiple signaling cascades and triggers apoptosis
74
Q

Side effects of drugs that inhibit proteosome (bortezomib and carfilzomib)

A
  • Thrombocytopenia, neutropenia, and/or anemia

- Peripheral neuropathy

75
Q

Drugs that inhibit HDAC

A

Romidepsin, vorinostat

76
Q

MOA of drugs that inhibit HDAC (romidepsin, vorinostat)

A

-Increase transcription and lead to cell cycle arrest and apoptosis.

77
Q

HDACs (histone deacetylases)

A

-work with histone acetyltransferases to regulate gene expression (acetylation associated with euchromatin and deacetylation associated with heterochromatin)

78
Q

What can cancer cells do to HDACs

A

Overexpress/abherrently recruit HDAC–>causes silencing of tumor suppressor genes

79
Q

Side effects of drugs that inhibit HDAC (romidepsin, vorinostat)

A
  • -HEMATOLOGIC (Pulmonary embolism, deep vein thrombosis)
  • -Drug-drug interations: severe thrombocytopenia and GI bleeding. PT and INR prolonged if given with Warfarin
  • Nausea, vomiting, diarrhea
  • Hyperglycemia
  • Fatigue, chills
  • Taste disorders
  • Mutagenic
80
Q

Differentiating agents

A
  • Tretinoin (ATRA, retin-A)
  • Arsenic trioxide
  • Bexarotene
81
Q

One hallmark of malignant transformation

A

Differentiation block

82
Q

Drugs that treat Acute promyelocytic leukemia

A

Tretinoin, arsenic trioxide

83
Q

Tretinoin (ATRA) mechanism

A

Promotes degradation of PML-RAR fusion protein, but doesn’t kill cells. Given with arsenic trioxide or anthracycline antibiotic to cause cell death

84
Q

Tretinoin (ATRA) toxicities

A
  • CNS toxicity
  • DIFFERENTIATION SYNDROME (fever, dyspnea, weight gain, pulmonary infiltrates)
  • Birth defects
  • Headache, dry skin, reversible hepatic enzyme abnormalities, bone tenderness, hyperlipidemia
85
Q

Arsenic trioxide MOA

A

Promotes cell death through apoptosis and necrosis. Given in conjunction with tetinoin to cause death of differentiated granulocytes

86
Q

Arsenic trioxide toxicities

A

Arrhythmias (prolonged QT). LEUKOCYTE MATURATION SYNDROME (similar to differentiation syndrome)

87
Q

Bexarotene MOA

A

-Selectively activates retinoid X receptors involved in regulation of cell growth and differentiation.

88
Q

Bexarotene use

A

Cutaneous T cell lymphoma

89
Q

Bexarotene pharmacokinetics

A

metabolized by CYP3A4

90
Q

Bexarotene side effects

A

GI symptoms, lipid abnormalities and pancreatitis

TERATOGENIC

IHO 4 (4 decks)

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