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Pharmacology Final > Chemotherapy Drugs II: Specific Drugs > Flashcards

Chemotherapy Drugs II: Specific Drugs Flashcards

1
Q

steroid hormones

A

induce apoptosis thru receptor activation

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2
Q

antimetabolites

A

interfere with anabolic process of generating nucleotide triphosphates for DNA synthesis

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3
Q

cross-linking agents

A

blocks strand separation and template processing thru intra- or interstrand interactions

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3
Q

topoisomerase inhibitors

A

interfere with enzymatic process of unwinding DNA

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4
Q

alkylating agents

A

interfere with replication machinery thru multiple mechanisms of altered binding and base recognition

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5
Q

anti-tubulin agents

A

interference with spindle fiber formation and separation of chromosomes into daughter cells during mitosis

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6
Q

targeted agents

A

block cancer associated pathways

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7
Q

immune modulators

A

block suppressors of immune targeting of tumors or activate immune cells to tumor surveillance

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8
Q

glucocorticoids MOA

A

bind to DNA, alter gene txn in response to hormone binding. direct lytic effect on malignant cells in lymphoid malignancies, leukemia, myeloma. ability to induce apoptosis dependent upon balance of pro and anti apoptotic proteins

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9
Q

side effects of glucocorticoids

A
  • metabolic effects: inc blood GLU, protein degradation
  • circulatory effects: inc cardiac output, inc sensitivity to catecholamines, inc renal Na+ retention
  • musculoskeletal effects
  • immune modulation
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10
Q

nitrogen mustard is what type of drug

A

alkylating agent

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11
Q

what is the common cellular target of alkylating agents?

A

crosslink DNA, cell cycle non-specific, so can bind DNA in any place of cell cycle. inhibits DNA synthesis thru damage to the nucleic acid template

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12
Q

MOA of alkylating agents

A

covalently binding to cellular macromolecules to inhibit DNA synthesis by damaging the nucleic acid template

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13
Q

side effects of alkylating agents

A

BAG: bone marrow suppression, alopecia, gastrointestinal

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14
Q

BAG effects

A

bone marrow suppression
alopecia
gastrointestinal
basically all the rapidly dividing cells

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15
Q

what type of drug is cyclophosphamide?

A

alkylating agent

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16
Q

cytoxan

A

cyclophosphamide

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17
Q

how is cyclophosphamide administered?

A

IV or oral

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18
Q

what is unique about cyclophosphamide?

A

it must be metabolized in liver to be active!! makes active metabolites phosphoramide mustard and acrolein

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19
Q

what is a negative sequelae of administering cyclophosphamide?

A

SHC: sterile hemorrhagic cystitis

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20
Q

what is cyclophosphamide used to treat?

A

lymphoma, sarcomas, mammary gland, mast cell tumor

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21
Q

what effects does cyclophosphamide have on cats?

A

GI effects more common in cats

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22
Q

cyclophosphamide causes GI effects more common in what species?

A

cats

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23
Q

what drug is not active until it is in the liver?

A

cyclophosphamide- must be metabolized in liver to be active!!

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24
Q

sterile hemorrhagic cystitis MOA

A
  • cyclophosphamide
  • acrolein damages bladder tissue when excreted in the urine
  • 10% of dogs develop SHC when treated with CP
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24
Q

T/F: you can give cyclophosphamide orally in addition to IV, but it will have decreased exposure to the “active drug”

A

false- oral dosing of CP has same exposure to active drug as IV, exposure to parent drug is decreased

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25
Q

you are treating a lovely golden retriever named Buddy for lymphoma with cyclophosphamide. you are very astute and remember from your CSU days that Buddy is at increased risk for sterile hemorrhagic cystitis. what are your options if this develops?

A
  • furosemide diuresis: increases clearance of acrolein in bladder
  • Mesna: decreases incidence by collecting in bladder and “capturing” the acrolein
  • switch to another alkylator like Chlorambucil
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26
Q

the owner of Buddy is concerned about potential GI effects of cyclophosphamide. what do you tell her?

A

not worried about them in Buddy because he is a dog; GI effects seen more commonly in cats

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27
Q

why would administering cyclophosphamide not be useful?

A

it is a pro-drug and requires metabolic activation by the liver

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28
Q

chlorambucil

A
  • alkylating agent, alternative to cyclophosphamide
  • oral only, delayed onset of action. metabolized to mustard
  • cerebellar toxicity ? brain fog?
  • used for chronic lymphocytic leukemia, lymphoma, mast cell tumors
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29
Q

melphalan (Alkeran)

A
  • alkylating agent
  • oral, active parent drug
  • multiple myeloma
  • active uptake by amino acid transporters
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30
Q

CCNU

A

Lomustine, CeeNU

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31
Q

CCNU (Lomustine, CeeNU)

A
  • oral, completely absorbed
  • crosses BBB by passive diffusion
  • myelosuppression, thrombocytopenia, hepatic toxicities associated with chronic use
  • mainly used for mast cell tumors and lymphoproliferative disorders in cats, but also in dogs with mast cell and histiocytic sarcoma too
32
Q

non-classic alkylating agents

A

dacarbazine and procarbazine
not 1st line drugs, likely won’t see
both act as methylating agents: inhibits DNA and RNA synthesis

33
Q

antimetabolites

A

interferes with cellular metabolism associated with making the building blocks of DNA and interfering with DNA and RNA synthesis

34
Q

ultimate effect of antimetabolites

A

purine/pyrimidine biosynthesis: depletes building blocks/things needed for making DNA

35
Q

what classes are included in the antimetabolites?

A
  • antifolates
  • 5-fluoropyrimidines
  • cytidine analogs
36
Q

methotrexate

A
  • antimetabolite, folate analog that blocks purine and thymidylate biosynthesis by inhibiting dihydrofolate reductase
37
Q

methotrexate toxicity

A

GI toxicity bc of enterohepatic recycling and it accumulates in GI tissue
not really used anymore

38
Q

cytosine arabinoside/ara-C, cytarabine

A
  • antimetabolites
  • analog to deoxycytidine, phosphorylated to ara-CTP because cells thing it’s cytadine
  • ara CTP is an inhibitor of DNA polymerase a: gums up works
39
Q

what is cytosine arabinoside/ara-C/cytarabine good for?

A
  • crosses into CNS: used for tumors that have potential CNS involvement!!
  • can be delivered as SC inj
  • makes things not H bond right; DNA helix won’t work right
40
Q

gemcitabine

A
  • antimetabolite, phosphorylated into many things
  • dFdCTP inhibits DNA polymerase: depletes deoxyribonucleotide pools thru inhibition of ribonucleotide reductase
  • incorporated into DNA strands is a toxic lesion X0
  • veterinary use is sparse, dosed IV
41
Q

5-Fluorouracil MOA

A
  • antimetabolite
  • gets in via facilitated transport, metabolized to phosphorylated forms
  • incorporated into both DNA and RNA: messes up synthesis and function
  • FdUMP depletes thymidine pools
  • metabolized to an inactive form by dihydropyrimidine dehydrogenase (DPD)
42
Q

what is 5-Fluorouracil used for?

A

treatment of epithelial tumors

43
Q

5-Fluorouracil is contraindicated in what species and why?

A

cats, deficiency in DPD leading to serious toxicity
(DPD is what metabolizes drug to inactive form)

44
Q

antitumor antibiotics

A

multiple MOA: form complexes w DNA, inhibit DNA/RNA synthesis, cell cycle nonspecific
BAG
most common used in vetmed!!

45
Q

single most active agent used in vet oncology

A

doxorubicin

46
Q

MOA of doxorubicin

A
  • inhibition of DNA/RNA polymerases
  • topoisomerase II inhibition
  • alkylation of DNA
  • reactive oxygen generation
  • perturbation of cellular Ca2+ homeostasis
  • inhibition of thioredoxin reductase
  • interaction with plasma membrane components
47
Q

metabolism of doxorubicin

A
  • widely distributed to tissues
  • metabolized hepatically and extra-hepatically
48
Q

toxicities of doxorubicin

A

GI, hematopoietic, cardiac***!!! associated w lifetime dose

49
Q

why should you be super careful w PPE when administering doxorubicin?

A

it is a severe vessicant, causing extravasation damage: if it comes out of blood and into tissue, that tissue will become necrotic and will kill tissue!!!

50
Q

what drug is known for its unique cardiac toxicities?

A

doxorubicin

51
Q

how does doxorubicin cardiac toxicity relate to dose?

A

cumulative cardiac toxicity is related to total lifetime dose (250mg/m^2)

52
Q

what is the best way to administer doxorubicin?

A

10-30 minute infusion times to decrease acute cardiotoxic events: acute cardiotoxicity has been observed with rapid infusion

53
Q

red death

A

doxorubicin

54
Q

doxorubicin summary

A
  • unique toxicities: cardiac in dog, renal in cat
  • most widely used drug in vet oncology
55
Q

what is doxorubicin toxicity in cats

A

renal

56
Q

dosing doxorubicin in small animals

A

A standard dose is 30 mg/m2 but for smaller dogs (<15 kg) and all cats a dose of 1 mg/kg is commonly used.

57
Q

doxorubicin in humans and dogs

A

similar variability observed, time-course of drug exposure is similar. not the DOSE, it’s the exposure and metabolism

58
Q

what is doxorubicin used for?

A

lymphoma, osteosarcoma, mammary gland tumors, thyroid, sarcomas

59
Q

other “rubicins” vs doxorubicin

A

epirubicin, daunarubicin, idarubicin (oral)
less cardiac toxicity, greater expense and generally not much of an advantage over doxorubicin

60
Q

mitoxantrone

A
  • antitumor abx
  • synthetic doxorubicin analog with similar MOA
  • not near as active in terms of generation of RO
61
Q

MOA of mitoxantrone

A

similar to doxorubicin, DNA intercalation and inhibition of DNA and RNA polymerases, topoisomerase II inhibition

62
Q

when do you use mitoxantrone?

A
  • used as cardiac-sparing drug in dogs that have reached cumulative max level of doxorubicin dosing, or that show cardiac abnormalities
  • primarily used in lymphoproliferative disorders and recently in TCC of bladder
63
Q

actinomycin D

A
  • antitumor abx
  • interacts w double-stranded DNA to block txn, binds to single-stranded to inhibit txn
  • inhibition of txn leads to inhibition of RNA and protein synthesis
64
Q

when do you use actinomycin D?

A
  • rapidly distributes, slowly eliminated
  • multi agent protocol use for lymphoproliferative disorders in relapse setting and as sub for doxo in dogs with cardiac abnormalities
65
Q

how are mitoxantrone and actinomycin D administered?

A

IV
both have BAG

66
Q

microtubule targeting

A

interfere with tubulin formation/function. cell cycle specific phase! M phase: doesn’t allow to separate or assemble

67
Q

what are the 2 classes of microtubule targeting drugs

A
  1. vinca alkaloids - pink periwinkle
  2. taxanes - japanese yew tree
68
Q

what is the difference between vinca alkaloids and taxanes?

A

vinca alkaloids prevent microtuble ASSEMBLY
taxanes prevent microtubule DISASSEMBLY

69
Q

vinca alkaloids drugs

A

vincristine and vinblastine

70
Q

vinca alkaloids uses

A
  • inhibit MT assembly, delivered by IV
  • vincristine is part of the CHOP protocol used in lymphoma
  • vinblastine is used for k9 mast cell tumors
71
Q

vincristine

A

antimicrotubule agent, vinca alkaloid
used for lymphoma in CHOP protocol

72
Q

vinblastine

A

antimicrotubule agent, vinca alkaloids
used for canine mast cell tumor txt

73
Q

taxane drugs

A

paclitaxel & docetaxel
- inhibit MT de-polymerization, delivered IV
- highly insoluble, so has to be given with another thing that causes hypersensitivity reactions. this has limited its use, but new formulations may change that !

74
Q

side effects of vincristine

A
  • peripheral neuropathy
  • minimal myelosuppression = AG of side effects
75
Q

side effects of vinblastine

A
  • IV! vessicant
  • BAG, less neurotoxicity
76
Q

which vinca alkaloid cures transmissible venereal tumor?

A

vincristine

77
Q
A
78
Q
A
79
Q
A

Pharmacology Final (9 decks)

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