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Pharmacology II > Lecture 36: Anti-Neoplastic Agents > Flashcards

Lecture 36: Anti-Neoplastic Agents Flashcards

1
Q

What are proto-oncogenes

A

Activating mutations, promote cell growth in the absence of cell signals

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2
Q

What are tumor suppressor genes

A

Inactivating genes, overrride checkpoints that prevent growth or cause cell death

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3
Q

Fraction of dividing cells in a tumor ___as tumor size increases

A

Decrease

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4
Q

What are the 2 contributions of mutations to cancer

A
  1. Acting on cancer cells
  2. Acting on micro environment
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5
Q

What are some examples of mutations acting on cancer cells

A

Genome instability and mutation, resisting cell death, deregulating cellular energetic, sustained proliferative signaling, enabling replicative immortality

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6
Q

What are some contributions of mutations acting on the micro environment

A

Evading the growth suppressors, avoiding immune destruction, tumor promoting inflammation, inducing angiogenesis, activating invasion and metastasis

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7
Q

What are some advantages of chemotherapy

A
  1. Tx diffuse disease
  2. Tx areas of difficult anatomical locations
  3. Improved sx outcome
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8
Q

What are some disadvantages of chemotherapy

A
  1. Solid tumors >1mg of tissue resistant
  2. Selection for resistant cells
  3. Adverse effects
  4. Expensive
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9
Q

What is the CHOP protocol for lymphoma

A
  1. Cyclophophamide
  2. Hydroxydanorubicin (doxorubicin)
  3. Oncovin (vincristine)
  4. Prednisone
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10
Q

What is the PD of alkylating agents

A

Convent bonding/cross linking to DNA bases (prefer guanine base), resulting in deletion of modified guanine bases during DNA replication and induce cell apoptosis

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11
Q

What stages of cell cycle to alkylating agents act on

A

All stages

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12
Q

Platinum alkylating agents are strongly absorbed by __, __ and __

A

Liver, bone, GI tissues

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13
Q

Which alkylating agents crosses BBB

A

Procarbazine and active metabolites of limestone

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14
Q

What alkylating agents are prodrugs

A

Dacarbazine, iomustine, cyclophosphamide

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15
Q

What alkylating agent is good for patients with liver issues and why

A

Melphalan because metabolized in plasma by hydrolysis

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16
Q

How are alkylating agents eliminated

A

Renal

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17
Q

What are the adverse effects of alkylating agents

A
  1. Vesication
  2. Dose-limiting toxicity
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18
Q

What is vesication

A

Severe tissue damage resulting from drug getting out of circulation

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19
Q

Which are at higher risk of vesication: pro-drugs or active dugs

A

Active drugs

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20
Q

What is dose limiting toxicity

A

Most severe toxic effect of the drug that does not lead to acute dead

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21
Q

Why is dose limiting toxicity the dosing goal for anti-neoplastic drugs

A

Kills the most cancer cells and reduces risk of developing resistant cancer cells

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22
Q

What is an adverse effect of lomustine

A

Cumulative myelosuppression

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23
Q

What is an adverse effect of cyclophosphamide

A

Necrotizing hemorrhagic cystitis

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24
Q

What alkylating agent causes lethal pulmonary edema in cats

A

Cisplatin

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25
Q

What is an adverse effect of carboplatin

A

Leukopenia

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26
Q

What is resistance mechanism against cyclophosphamide

A

Aldehyde dehydrogenase inactivates drug

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27
Q

What are some resistance mechanisms common to all alkylating drugs

A
  1. Increased expression of DNA repair enzymes
  2. Increasing expression of P-gp
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28
Q

Melphalan is taken up by the __transport system and therefore reducing expression of enzymes in that transport drug can cause resistance

A

Leucine

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29
Q

Mechlorethamine is taken up by __transport system and therefore reducing expression of enzymes that transport drug can cause resistance

A

Chlorine

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30
Q

What are anthracyclines- doxorubicin, mitoxantrone, and dactinomycin used to tx

A

Canine lymphoma

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31
Q

What is PD for doxorubicin

A

Combines with iron and catalyzes generation of oxygen radicals causing DNA damage leading to apoptosis, lipid perioxidation of cell membrane

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32
Q

Doxorubicin and mitoxantrone inhibit __ and therefore block __ and reduce ___

A

Topoisomerase II, DNA replication, RNA/protein synthesis

33
Q

Dactinomycin inhibits ___

A

DNA dependent RNA synthesis

34
Q

Where does doxorubicin, mitoxantrone and dactinomycin act in cell cycle

A

All phases

35
Q

Anthracyclines- doxorubicin, mitoxantrone, and dactinomycin are excluded from CNS by __ and therefore problem in ___

A

P-gp, collies

36
Q

How are anthracyclines metabolized

A

Hepatic

37
Q

How is doxorubicin eliminated

A

40-50% in feces, 10% in urine

38
Q

How is mitoxantrone eliminated

A

100% drug eliminated unchanged in urine

39
Q

How is dactinomycin eliminated

A

Unchanged in urine and feces

40
Q

What are some early adverse effectives of doxorubicin

A

Nausea, vomiting, anaphylaxis, ventricular arrhythmia

41
Q

What are some intermediate adverse effects of doxorubicin

A

Alopecia, thrombocytopenia, neutropenia, vesication

42
Q

What drug can be used to mitigate vesication caused by doxorubicin

A

Dexrazoxane

43
Q

What are some chronic adverse effects in dogs associated with doxorubicin and how does it happen

A

DCM- oxygen radicals damage cardiomyoctes in SR

44
Q

What type of dogs are more susceptible to DCM from doxorubicin

A

ABCB1-/- (collies)

45
Q

What are some chronic adverse effects in cats with doxorubicin and how does it happen

A

Chronic renal failure - oxygen radicals damage podocytes of renal glomeruli

46
Q

What are some adverse effects of dactinomycin

A

Myelosuppression, diarrhea, ulcerative stomatitis, urate sone formation in dogs with SLC2A9 mutation (Dalmatians), vesicant

47
Q

What are some mechanisms of resistance to anthracyclines

A
  1. Increased P-gp expression
  2. Increased glutathione- reduces free radical production
48
Q

What is the PD for nucleotide analogs- cytarabine, gemcitabine

A

Incorporated into growing DNA strand during S phase, DNA polymerase can;t read modified sugars, resulting in death of daughter cells

49
Q

You can only give gemcitabine ___only

A

IV

50
Q

How is cytarabine and gemcitabine metabolize

A

Converted to Ara-U in liver and kidneys by cytosine deaminase

51
Q

What are some adverse effects of cytarabine and gemcitabine

A

Myelosuppression- leukopenia most common, anemia, thrombocytopenia

52
Q

How does resistance develop to cytarabine and gemcitabine occur

A
  1. Increased P-gp
  2. Increased expression of cytosine deaminase
53
Q

What is rabacfosadine labeled for

A

Canine lymphoma

54
Q

What is the PD for rabacfosadine

A

Guanine analog incorporated into DNA chain of replicating cells, does not have ribose base that DNA polymerase recognizes and terminates DNA replication in S phase

55
Q

What are some adverse effects of rabacfosadine

A

Pulmonary fibrosis, tachypnea, cumulative dermatology, bone marrow suppression, GI effects, lethargy, tachycardia

56
Q

What are some CI of rabacfosadine

A
  1. Existing pulmonary fibrosis
  2. Chronic pulmonary disease
  3. West Highland White Terriers
57
Q

What is the PD for vincristine, vinblastine, paclitaxel

A

Act to stabilize microtubules, prevent proper breakdown of mitotic spindle during cytokinesis and induce apoptosis during M phase of cell cycle

58
Q

Vincristine and paclitaxel sites of action differ, theses drugs act __

A

Synergistically

59
Q

Vincristine, vinblastine and paclitaxel are excluded from CNS via __, therefore problem in ___

A

P-gp, collies

60
Q

Which one has more CNS toxicity: vincristine or vinblastine

A

Vincristine

61
Q

How is vincristine, vinblastine and paclitaxel metabolized

A

Hepatic

62
Q

How is vincristine, vinblastine, and paclitaxel eliminated

A

GI, biphasic, slow elimination

63
Q

What is an adverse effect of vincristine

A

Neurotoxicity- interaction with axonal microtubules

64
Q

What is an adverse effect of paclitaxel

A

Histamine release

65
Q

Which is more myelosuppressive: vinblastine or vincristine

A

Vinblastine

66
Q

What is C-kit

A

Receptor tyrosine kinase that drives leukopoesis, induces cell cycle activation, protein synthesis

67
Q

C-kit has greatest proliferative effects on __cells and therefore is a proto-oncogene in __

A

Mast cells, canine mast cell tumors

68
Q

What is Toceranib indicated for

A

Mast cell tumors

69
Q

What is the PD for toceranib

A

Competitive antagonist of ATP binding to the kinase domain of C-kit at G1 phase of cell cycle

70
Q

What are some adverse effects of toceranib

A

GI, bone marrow suppression (anemia, neutropenia), changes in coat color, thromboembolic dz and inappropriate bleeding

71
Q

What is L-asparginase used to tx

A

Lymphoma

72
Q

What is the PD of L-asparaginase

A

Blocks conversion of aspartame to asparagine in G1 phase of cell cycle

73
Q

You cant give L-asparaginase __because it can cause fatal anaphylaxis

A

IV

74
Q

How is L-asparagine metabolized and eliminated

A

Hydrolyzed to amino acids and used for new protein synthesis

75
Q

What are some adverse effects of L-as-arginine

A

Pruritus, urticaria, dyspnea, hypotension, vomiting, diarrhea, hepatoxicity, defective coagulation production, hyperglycemia

76
Q

How does prednisone work

A

Induces apoptosis of most immune cell linages

77
Q

What is the DOC for TCC

A

Piroxicam

78
Q

What is the PD for piroxicam

A

Nonspecific cyclooxygenase inhibitor, induces tumor cell apoptosis by reducing angiogenesis

79
Q

What are some adverse effects of piroxicam

A

GI ulcerative and renal papillary necrosis

Pharmacology II (36 decks)

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