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IHO week 4 > Antineoplastics IV > Flashcards

Antineoplastics IV Flashcards

1
Q

Mechanism of resistance for vinca alkyloids:

A

decreased accumulation via increased P-glycoprotein expression

changes in target proteins**mutations in tubulin that prevent binding

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2
Q

Chemo regimens and specific diseases for vincristine:

A

MOPP – Hodgkin’s disease

CHOP – non-Hodgkin’s lymphoma

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3
Q

Specific regimens and disease for vinblastine:

A

ABVD – Hodgkin’s disease

PVB – testicular cancer

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4
Q

Most significant toxicity of vincristine:

A

CNS toxicity

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5
Q

Most significant toxicity of vinblastine:

A

Bone marrow suppression

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6
Q

Why is depression of deep tendon reflexes seen within 2-3 weeks in 100% of patients being treated with vinca alkyloids?

A

This is used as an indication of sufficient dose

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7
Q

What is used as an indication to decrease the dose of vinca alkyloids?

A

severe paresthesias (pins and needles) and mild to moderate sensory loss

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8
Q

MOA for taxanes?

A

bind to tubulin and enhance and stabilize spindle assembly

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9
Q

Mechanism of tumor cell resistance to taxanes?

A

decreased accumulation via increased P-glycoprotein expression

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10
Q

Metabolism of taxanes?

A

CYP450

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11
Q

Unique toxicities of taxanes?

A

hypersensitivity

peripheral neuropathy

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12
Q

Vinca alkyloid used with Capecitabine (similar to 5-FU) as 3rd line tx of breast cancer?

A

Ixabepilone

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13
Q

Why is Ixabepilone 3rd line for bresat CA?

A

DOES NOT produce multidrug resistance

** used after pts have failed anthracycline abx and taxane tx

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14
Q

Main result of using glucocorticoids in chemo?

A

immunosuppression

**decreased IL-2 and TNF-a

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15
Q

Cyclosporine

Class:

MOA:

Result:

A

Immunosupressive antibiotic

binds cyclophilin to to inhibit calcineurin

decreased release of IL-2 –> decreased T-cell proliferation

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16
Q

Tacrolimus

Class:

MOA:

Result:

A

Immunosuppressive antibiotic

binds FK-binding protein to inhibit calcineurin

decreased release of IL-2 –> decreased T-cell proliferation

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17
Q

Two immunosuppressive abx that inhibit mTOR making them anti-angiogenic and anti-proliferative:

A

Everolimus

Temsirolimus

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18
Q

Antibodies targeting CD20 in B-cell non-Hodgkin’s lymphoma:

A

Rituximab

Ibritumomab (90Y)

Tositumomab (131I)

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19
Q

Anitbodies targeting CD52 in B-cell chronic lymphocytic leukemia:

A

Alemtuzumab

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20
Q

Fusion protein that has diptheria toxin coupled to IL-2

  • inhibits protein translation by inactivating EF2
  • goal is to kill IL-2 receptor expressing cells (activated T’s B’s and Mac’s)
  • approved for use in cutaneous T-cell lymphoma
A

Denileukin Diftitux

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21
Q

General half life length of antibodies?

A

LONG (3-6 mos)

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22
Q

Toxicities of antibody tx:

A

infusion rxn

hypersensitivity (ie. HAMA)

infections (ie. reactivation of latent TB)

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23
Q

Specific toxicities for anti-CD antibodies:

A

cardiac arrhythmias

tumor lysis syndrome

24
Q
  • short half lifes
  • not cytotoxic
  • recruit immune cells to do the actual killing
A

cytokines

25
Q
  • induces T-cells
  • half life = 13 min
  • used to induce LAK or CIK cells
A

IL-2

26
Q

Big side effects of IL-2?

A

cytokine storm

palmar-plantar erythrodysesthesia

fatal hypotension

27
Q

Decrease production of fibroblast growth factor (FGF)

inhibits cell division of both normal and tumor cells

increases MHC I expression on tumor cells

A

IFN-a

28
Q

What is a function of FGF?

A

angiogenesis

29
Q

Side effects of INF-a?

A

depression (mechanism not understood)

flu-like sx

hypotension

myelosuppression

30
Q
  • causes fibroblast proliferation
  • chemokine induction (IL-6, IL-8) and T/B cell activation
  • SHORT half life (1-2 min)
  • *intra-arterial administration

-decreases proliferation of tumor cells while sparing normal cells

A

TNF-a

31
Q

Dose limiting toxicity of TNF-a?

A

malaise and flu-like sx —> hemorrhagic necrosis

32
Q

Stimulates production of RBCs?

A

erythropoietin

33
Q

Stimulates production of neutrophils?

A

Filgrastim (G-CSF)

34
Q

Stimulates production of granulocytes, eosinophils, basophils and monocytes?

A

Sagramostim (GM-CSF)

35
Q

Stimulates production of platelets?

A

IL-11

Thrombopoietin

36
Q

Tyrosine kinase STIs of Bcr-Abl:

Cancer type:

A

Bosutinib

Dasatinib

Imatinib

Nilotinib

**CML

37
Q

Tyrosin kinase STIs of EGFR:

Cancer type:

A

Cetuximab

Erlotinib

Gefitinib

Panitumumab

**epithelial derived (lung, pancreas, head and neck, breast, prostate, colon, stomach, ovaries and brain)

38
Q

Tyrosine kinase STIs of HER2:

Cancer type:

A

Pertuzumab

Trastuzumab (ADO-Trastuzumab Emtansine)

**breast

39
Q

Tyrosine kinase STIs of PDGF-R, VEGF-R:

Cancer type:

A

Pazopanib, Sorafenib, Sunitinib

**many

40
Q

Tyrosine kinase STIs of c-kit:

Cancer type:

A

Dasatanib

Imatinib

Nilotinib

Sunitinib

**GIST

41
Q

binding of the antibody interferes with HER2 signaling

identifies HER2 overexpressing cells as foreign so they can be destroyed by the immune system

A

Trastuzamab

42
Q

first DIMERIZATION inhibitor

prevents HER2 from dimerizing with other HER2 receptors

A

Pertuzumab

43
Q

internalized and undergoes lysosomal degradation to form two components:

A

ADO-Trastuzumab Emtansine

forms:

  • trastuzumab
  • DM1 — small molecule that disrupts microtubules by binding tubulin
44
Q

Toxicities of antibodies:

A

Hypersensitivity rxns

HAMA

infx

birth defects/fetal loss

***ventricular dysfunction and CHF

45
Q

Deprives tumor cells (some ALL cells lacking asparagine synthase) of asparagine:

A

L-Asparaginase

**cause hypersensitivity rxn

46
Q

Reversible inhibitor of 26S proteasome triggering apoptosis:

A

Bortezomib

47
Q

Irreversible inhibitor of 26S proteasome triggering apoptosis:

A

Carfilzomib

48
Q

Side fx of Bortezomib and Carfilzomib:

A

thrombocytopenia, neutropenia, anemia

peripheral neuropathy

49
Q

HDAC inhibitors increase transcription and lead to cell cycle arrest and apoptosis:

A

Romidepsin

Vorinostat

50
Q

Side effects of HDAC inhibitors:

A

Pulmonary embolis, DVT

Drug interactions (increase efficacy of Warfarin)

N/V

hypERglycemia

fatigue, chills

dysgeusia, dry mouth

51
Q

Promotes cell differentiation (ie. APL w/ t(15;17)):

A

Tretinoin (ATRA)

**doesn’t kill cell, must be followed by arsenic trioxide or anthracycline abx

52
Q

Toxicities of ATRA:

A

CNS (dizziness, anxiety, depression, confusion, agitation)

Differentiation syndrome (fever, weight loss, dyspnea, pulmonary infiltrates)

birth defects

53
Q

heavy metal toxin promotes cell death through apoptosis and necrosis

A

Arsenic Trioxide (ATO)

54
Q

Toxicities of ATO:

A

arrythmias

leukocyte maturation syndrome

55
Q

Selectively activates retinoid X receptors

approved for cutaneous T-cell lymphoma

metabolized by CYP3A4 (potential for many drug interactions)

A

Bexarotene

56
Q

Side effects of Bexarotene:

A

lipid abnormalities in pancreas

GI sx

Teratogenic

IHO week 4 (13 decks)

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