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Anti-Neoplastics Flashcards

1
Q

What are the mechanisms that anticancer drugs act on?

A

1) damage DNE
2) Inhibit synthesis or funtion of DNA
3) ACtion on Mitotic Spindle
4) targeted DRUGS (MABs, NIBs, and mTOR inhibitors)

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2
Q

Cell cycle spefic drugs

A

most effective in the certian phases of the cell cycle

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3
Q

cell cycle NON specific

A

their targets are present in both the cell cycle and resting cells

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4
Q

What are alkylating agents?

A
  • moiety bound to DNA to stop cell cycle
  • Nitrogen mustards
  • Alkyl sulfonates
  • Nitrosoureas
  • Aziridines
  • Antibiotics
  • Platinum drugs
  • Triazenes
  • Hydrazines
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5
Q

What is adjuvant therapy?

A

given to activate the immune response after surgery

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6
Q

What is neoadjuvant therapy?

A

given to debulk the tumore, and remove tumor cells from the inffected site

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7
Q

What is Tumor lysis syndrome (TLS)

A

a multi-factorial process,

  • the lysis of tumor cells relases purine nucleic acids K+ and P
  • get renal saturation due to elimination
  • uric acid deposites with calciump
  • volume depetion, tubular obstruction, cytotoxic chemotherapy
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8
Q

How do you manage TLS?

A

hydration!!!!
allopurino to prevent uric acid formation
Rasburicase to degrade uric acit to water soluble allantoin for elimination

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9
Q

What are teh bischloroethylamine alkylating agents?

A 
cyclophosphamide
ifosfamide
merchlorethamine 
melphalan
chlorambucil
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10
Q

What are the mechanisms of the bischloroethylamine alkylating agents?

A
  • transfer alkyl group ot DNA
  • N7 guanine
  • ss or ds DNA cross-linking DNA modified
  • Resulting in miscoding; strand breakage via guanine excision
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11
Q

What are the resistance mechanisms of the bischloroethylamine alkylating agents?

A

-v uptake
v activation
^ inactivation (conjugation) of reactive moiety (^rate& capactity) or ^ repair of DNA miscodes

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12
Q

What are adverse effects of the bischloroethylamine alkylating agents?

A
  • does-related toxicites
  • direct vesicant action (avoided where orally acitve)
  • eps toxic to rapidly dividing cell populations (bone marrow, GI, Reporductive systems, alopecia)
  • N/V (use 5HT3 antagoinist)
  • CNS(ifosfamide– chloroactealdehyde)– altered mental status etc
  • Lungs (ALL ALKYLATING AGENTS esp cyclophosphamide, chlorambucil, melphalan
  • — fibrosis, dyspenea, cyanosis, pulmonary insufficiency
  • carcinogenity- lekemias and solid tumors (secondary malignacies)
  • Renal failure (cyclophosphaamide and ifosfamide)
  • Urotoxicity/bladder tumore (acrolein released by cyclophosphamide and ifosfamide)
  • – sever hemorrhagi cycstitis (MENSA prevents)
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13
Q

What is Mesna and what does it prevent?

A

a phophylatic chemoprotectant from hemorrhagic cystitis

-IV/oral

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14
Q

What does cyclophosphamide do and when is ti used?

A

total immune system ablation

used for allogenic stem cell transplantation, and RA

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15
Q

What are the alkyl sulfonates?

A

Busulfan

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16
Q

What are the toxicities, of busulfan?

A

myelosuppression, at conventional doses
pulmonary fibrosis
GI damage
Veo-occlusive diseasze of the liver, increased by coincident cyp inhibitors
asthenia and HYT resembing addison’s disease

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17
Q

What are the Nitorsoureas?

A

Carmustine and Lomustine (both akylators)

-carmustine decompostition products carbamolyate proteins– inhibit DNA repair

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18
Q

Is cross resistance with other alkylating agents comon for hte nitrosoureas’?

A

NO!!

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19
Q

What is the distributation of the nitrosoureas’?

A

enter CNS in measurable concentrations b/c hygly lipophilic & non-ionized at physicologic pH

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20
Q

What are the toxicities for the nitrosoureas’?

A

thromobcytopenia, leucopenia, N/V, administration site rxns
pulmonary fibrosis
endocrine dysfunction with brain irradiation
– hyperprolactinemia, and hypthyroidism (v throxin T4)
-encephalopathy and seizures
^ transminases, alkalin phosphatase, and hyper bilirubinemia

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21
Q

What is thiotepa and what are its toxicities?

A

a polyfunctional aziridine alkylator

  • forms intersrand cross-links of DNA
  • lipophilic (IV, IVe, or IC)
  • Toxicities: myelosuppression, neurooxic, injection site rnx, dysuria, urinary urgency, urinary retention, chemical or hemorrhagic cystitis
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22
Q

What is mitomycin and what does it do?

A 
a bioreductive alkylating agent
-metabolically activated under reducing contictions (hypoxic solid tumor)
-superoxide free radical generation 
-bone marrow suppression (slow recovery)
Injection site rns (hemolytic anemia)
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23
Q

What are the platinum drugs?

A

cisplatin, carboplatin, oxaliplatin

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24
Q

What does cisplatin do?

A

-intrastand DNA links with N7 guanine,
The DNA relication and transcription interrupted (breaks and miscoding, P53/checkpoint proteins -> induction of apoptosis)

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25
Q

What are the toxic effects of cisplatin?

A

nephrotoxic!!! (amifostine a cytoprotective agent!!!)
Ototoxicity (hearing loss)
mild to mod- myelosuppression
marked N/V (ondansetron + steroids + aprepitant (NK-1 antagonist))
porgressive peripheral, motor & sensory neuropathy

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26
Q

What is Dacarbazine?

A

a triazine DNA methylating agent (O6 guanine)

resistance due to removal of methyl groups form teh O6 guanine bases by AGT

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27
Q

What are the toxicites of Dacarbazine?

A

Myelosuppression; leukopenia, thrombocytopenia,

N/V

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28
Q

What are the DNA methlyating agents?

A

Trazewnes and Hydrazine

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29
Q

What is procarbazine and what is its mechanism?

A

a highly reactive DNA methylaor via CYP activation – causes damage via creaks and translocations

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30
Q

What is the resistance to procarbazines?

A

rapid when use as a single agent due to guanine repair via guanin-O6-alky transferase, and also lacks cross-resistance with other mustratd-type alkylators

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31
Q

What are the adverse/ toxicities seen with procarbazine?

A 
leukopenia and thromobytopenia
-Mild N/V
-Weak MAO inhibitor , hypertensive DDrns
-Disulfiram-like actions (alcohol ingestion to be avoided)
potent immunosuppressive
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32
Q

What are the antimetabolites?

A
  • folic acid analogs
  • pyrimidine analogs
  • purine analogs and related inhibitors
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33
Q

What are the folic acid analogs?

A

Methotrexates

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34
Q

What are the pyrimdine analogs?

A

Fluorouracil (5-FU)
capecitabine
Cytarabine
Gemcitabine

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35
Q

What are the purine analogs and related inhibitors?

A

Pentostatin
cladridine
Fludarabine

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36
Q

What is methotrexates mechanism?

A

a DHFR inhibitor, adn is trapped in cell due to polyglutamated

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37
Q

What is important about the methotrexate mechanism, due to THF?

A

methotrexate deplets the THF from all cells and thus must use Leucovorin to rescuce the cells that are not tumor cells,

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38
Q

What are the other methotrexate analogs?

A

Pemetrexed

Trimetrexate

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39
Q

What are the toxicites of methotrexate?

A

GI, N/V, abdominal distress

  • Bone marrow, anemia, lymphoproliferative disorders
  • weak acid; hydrate adn alkaliinize urine
  • pneumonitis
  • anemia in RA or psoriasis (MTX and 5-FU)
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40
Q

What are the resistance mechanisms for MTX?

A

V uptake/^ efflux; V polyglutamation

-^ DHFR enxyme levels & or modified structures

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41
Q

What is 5FU mechanism?

A

Inhibits DNA synthesis by “thymineless death” (FdUMP)
incorporated into DNA to inhibit synthesis and function (FdUTP)
interference with mRNA translation (FUTP)

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42
Q

What are the resistance mechanisms for 5-FU?

A

V activation of 5-FU; muation of TS; upregulation of TS (feedback b/c unbound enxyme inhibitis own mRNA)

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43
Q

What are the toxicites of 5-FU?

A

Acute chest pain (ischemia)
myelosuppression, anemia, mucositis, diarrhea,
-Hand and foot syndrome!!! – peripheral neuopathy!!!!!!!

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44
Q

What is the interaction with leucovorin?

A

5-FU: increase formation of TS complex and enchances the response to 5-FU
MXT: given as a THF rescue

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45
Q

What is Capecitabine, and how is it similar/differnt from this durg?

A

a pre-drug of 5-FU

-similar toxicities!!! (hand-foot syndrome ^ in frequency)

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46
Q

what is the mechanism of cytarabine?

A

a antimetabolite, pyrimide analog

  • converted to ARA-CTP
  • – the 2’hydroxyl hinders 3-D bond rotation; interferes with base stacking
  • inhibition of chain elongation (leads to shortened DAN strands)
  • Multiple DNA strand duplications (increase recombination possibilites)
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47
Q

What are the resistance and toxicites for cytarabine?

A

Resistance: V cellular uptake; decreased ARA-C conversion to ARA-CTP; or increased ARA-CTP to ARA-UMP (inactive)
Toxicitiy: potent myelosuppressive agent; severe leukopeina, thromovytopenia, and anemia, megaloblastic changes
-GI, and noncardiogenic pulomary edema

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48
Q

What is Gemitabine?

A

has an additional bp, and the repair is more difficult
-better penetration/retention; affinity for dinase
Toxicity is myelosuppresion, flu like symptoms and ^ liver transaminases

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49
Q

What is mercaptopurine’s resisances?

A
  • v or complete lack of HGPRT
  • ^alkaline phosphatase activity
  • v drug uptake and ^ efflus
  • altered enxyme sturcture
  • altered recognition of DNA breaks
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50
Q

DDI with mercaptopurine?

A

Allopuinol!!! must reduce does to avod excessive toxicity!!!

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51
Q

What is the benifit of TPMT genotyping with mercaptopurine administration?

A

if low TPMT leves will have to use ^ does of drug to be benificial

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52
Q

What is thioguanine?

A

similar mechanism of action as 6MP (RNA & DNA synthesis inhibition; incorporation of thio-nulecotide into RNA and DNA), with similar resistance mechanisms

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53
Q

What is the mechanism of fludarabine & cladribine?

A

-rephosphorylated intracellularly ot acitve triphosphate derivative (resistance; v enxyme activeity – not P)
-inhibits DNA synthesis & ribonucleotide reductase
-activeates apoptosis (acive agains indolent disease
they have long lasting effects

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54
Q

What are the natural products?

A

Plant alkaloids and mold products

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55
Q

What are the vinca alkaloids?

A

Vincristine
Winblastine
Vinorelbine

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56
Q

What are the amptothecin analgos?

A

Topotecan

Irinotecan

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57
Q

What are the podophyllotoxins?

A

Paclitazel

Docetaxel

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58
Q

What are the anthracyclines?

A 
Doxorubicin
Daunorubicin
Epirubicin
Idarubicin
Mitoxantrone
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59
Q

What are the Bleomycins

A

Bleomycin

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60
Q

What are the actinomycins?

A

actiomcin D

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61
Q

What are the asparaginase?

A

asparaginase

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62
Q

What is extravasataion toxicity?

A

Excape of drug from vascular causeing excessive toxicity (localized) and loss of tissue which can be devilitating and plastic surgery to correct

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63
Q

What is the mechanism of the vinca alkaloids?

A

they bind specifically to b-tublin and block tubulin (alpha and beta) polymerization
-this arrests cells in metaphase (apoptosis)

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64
Q

What is the resistance of vinca alkaloids?

A

-P-glycoprotien, MRP, BCRP
— b-tubulin mutations (the binding site)
efflux protein actiators

65
Q

What is the toxicites for the vinca alkaloids?

A

neurotoxicity— due to the presance of microtubules in the CNS

  • allopecia
  • leuokpenia not with vincrstine
  • peripheral neuropathy!!! (tingling in hands and feet)
66
Q

What is the relationship b/ taxols adn vinca alkaloids?

A

both act on the b-tublin
Taxols- prevent disassembly
vinca alkaloids- prevent polymeriation (loss of activity)
and they bind to specific stide on the b-tubulin (also colchicine in tx of gout)

67
Q

What is the mechanism of camptothecin analogs?

A
  • stabilize DAN-topo I cleavable comoples

- - ssDNA breaks and dsDNA breaks

68
Q

what are the resistance mechanisms of irinotecan and topotecan?

A
  • G2 arrest correlates with v drug sensitivity

- invitro: ^ efflux (p-gp, MRP) mutation or ^ expression of topo-I or topo-II

69
Q

What is the difference in excreation of irinotecan and topotecan?

A

Irinoteacn: hepatic metabolism (UGT polymorphisms impact clinical use– V conjugation=^ neutropenia)
– with severe toxicity in pts with Gilbert syndrome
Toptecan: renal elimination (dose adj.)

70
Q

What are the toxicites of topotecan?

A

neutropenia +/- thrombocytopenia

-cuscositis and diarrhea, N/V elevated hepatic enzyems

71
Q

What are the toxicites of irinotecan?

A

dose limiting diarrhea!!!

  • 24 hr: Loperamide effective except in sever cases, rarely fatal
  • myleosuppression: anemia, leukopenia, neutorpenia
  • N/V, nucositis, alopecia
  • elevation in hepatic enxymes
72
Q

What is the mechanism of Etoposide and teniposide?

A

they complex with topo-II and DNA

73
Q

What are the resistacne mechanisms of etoposide and teniposide?

A

^ efflux; mutation or v topo-II (P53 mutation)

74
Q

What are the differing routes of admistration and toxicites, with eliminations for the Topo-II inhibitors?

A

Etoposide- oral, renal elimation ; dose adjust; myelosuppression and alopecia
Teniposide- IV; extensive metabolism; myelosuppression & N/V

75
Q

What is Paclitaxel and Docataxel’s mechanisms?

A

bind to b-tubulin and antagonize disassembly

76
Q

What are the resistance mecaninsme for the taxols?

A

efflux; mutation of targert

77
Q

What is important about paclitazel (IV taxol)?

A

cermaphor casues hypersensitivity; and can be treated by prophylactic antihistamine and steroids

78
Q

What is improtant about Docataxel(IV docetaxel)?

A

polysorbate 80 is disolving and has a lower incidence of hypersensitivity

79
Q

how are the taxols metabolized?

A

extensivly via CYP metabolism (paclitaxel clearance is not dose linear – cremaphor)

80
Q

What are the toxicites for the taxols?

A 
Paclitaxel: (bone marrow suppression, myalgias & stokcing-glove sensory neurophathy, mucositis)
Docetazel toxicity (more severe, but short-lived, neutropenia, peripheral/ pulmonary edema; progressive with duration -- prophylactic oral dexamethasone)
81
Q

What are the important mechanism of hte Anthracyclins?

A

1) intercalate with DNA, affecting transcription and replication
2) ceomplex with TOPO-II and DNA
3) free radicals from semiquinone

82
Q

What are the resistance mechanisms of the antracyclines>?

A

^ efflux
^ glutathion peroxidase (free radical scavenger)
v topo or mutation
^ repair efficiency

83
Q

What are the toxic effects of aunorubicin, Doxorubicin, Epirubicin and Idarubicin?

A

myelosuppression stomatitis, alopecia, GI disturbances (extravasational necrosis)
***Acute (reversible): tachycardia, arrhythmias, hypotension,v ejection fraction, troponin-T release
Chronic (irreversible) CHF – max dose 500mg/m2 ( may requrie a hrt transplant)
Protection with dexrazoxane, iron chelatin agnet

84
Q

What drugs produce red urine?

A

any systemic drugn (danunorubicin, doxorubicin, epirubcin, idarubicin)

85
Q

What drug produces blue urine?

A

Mitoxantrone

86
Q

What is mitoxantrone’s mechanism of action?

A

intercalates DNA and inhibitos TOPO-II (ss and ds breaks)

87
Q

what is mitoxantrone’s toxicity?

A

myelosuppression, cardiotoxicity, mucositis, stomatitis, alopecia
Cardiotoxicity (Dox/Dauno similarities)

88
Q

What drug-Fe complex oxidizes deoxyribose of thymidylate adn other nuclotides?

A

Bleomycin,

ss and ds DNA breaks

89
Q

What is the resistance to Bleomycin?

A

degradation by specific hydrolase (low activity skin & lung)

v uptake, adn ^ rtepair, ^ inactiavactivation

90
Q

What are the toxicities to Bleomycin?

A

Pulomary toxicity, dry cough–> fibrosis
hyperpigmentation, hyperkeratosis, erythema, ulceration (low activity of degenrative hydrolase in these areas)
<myelosupperssion

91
Q

What druge intercalates DNA (adj G-C base pairs)

A

AntinomycinD

92
Q

What type of DNA breaks doe Actinomycin-D do?

A

ssDNA via fre-radical and TOPO-II action

93
Q

What are the toxic effects of Actinomycin-D

A

Pancytopenia, anorexia, N/V
Mucositis, Diarrhea, alopecia, extravasation necrosis
-erythema, desquamation, inflammation and pigmentation in areas previously or concomitantly, x-rayed (skin toxicity)

94
Q

What does L-Asparaginase do?

A

and enzyme form E. Coli
that converts Asp–> Aspartic acid adn ammonia
helps to stop lymphid cancer

95
Q

What is the resistacne to L-asparaginase?

A

increase asparagin synthatse

96
Q

What can L-Asparaginase caseue?

A

Pancreatitis: necrotic/inflammatory

Has a potentiallyl fatal hypersentitivy

97
Q

What are the Miscellaneous Agents?

A

Hydroxyurea,

Thalidominde

98
Q

What are the differntiating Agents?

99
Q

What are the immunosuppressants?

A

Glucocorticoids

Dexamethasone

100
Q

What are the EGFR antibodies?

A

Gemtuzumab
Tratustuzumab
Cetuximab
Panitumumab

101
Q

What are the VEGF antibodies

A

Bevacizumab

102
Q

What are the antibodies to CD20?

A

Rituximab

Ofatumumab

103
Q

What are the antibodies to CD52

A

Alemtuzumab

104
Q

What are the radiolabeled drugs?

A

Ibritumumab

Toistumomab

105
Q

What are the TKIs?

A

Imatinib Dasatinib

106
Q

Waht are the EGFR TKIs?

A

Gefitinib
Erlotinib
Lapatinib

107
Q

What are th eBCR-ABL TKIs?

A

Imatinib
Dasatinib
Nilotinib

108
Q

What are the VEGF TKIs?

A

Suntiinib
Sorafenib
Pazopanib

109
Q

What are the proteosome inhibitors?

A

Bortexomib

110
Q

What are the mTOR inhibitors

A

Sirolimus
Everolimus
Temsirolims

111
Q

What is Hydroxyureas?

A

a oral free radical scavanger
stops at the rate limiting step in DNA synthesis, and prevent DNA replication and cell synthesis
catalytic center of ribonucleotide reductase subunit

112
Q

What are the resistance mechanism for hydroxyurea?

A

upregulation of reductase

113
Q

What is hydroxyurea used as?

A

a mylosuppressive or radiation sensitizer

114
Q

What is thalidomide, an what did it previously get used for?

A
  • is an anti-cancer drug
  • -inhibits tumore cell proliferation
  • -inhibits tumor cell adhesion to stroma
    • inhibitos angiogenesis
  • -Enhances NK cell activity
  • used to be used for deditive in pregancy
115
Q

What are the toxicities of Thalidomide or lenalidomide?

A

tx-emergent peripheral sensory neuropathy, sedation, constipation

116
Q

What are the adrenocorticosterodis?

A

prednisone, dexamethasone

117
Q

What is the mechanism of Tretinoin?

A

disrupts gene and promotes differnetiaon

is a teratogen so avoid during preg…

118
Q

What is retinoic acid syndrom?

A

characterized by fever, dyspenea, weight gain, pulmonary inflitarates, and pleural or pericardial effusions

119
Q

What are the targeted therapies?

A

cell surface recptor antibodies
receptor tyrosine kinase inhbitors
mTOR inhibitors
PI3L inhbitors

120
Q

What are the cell surface receptor antibodies?

A
  • EGFR

- VEGF

121
Q

What are the RTKIs?

A
  • multi-receptor

- single-receptor

122
Q

What does trastuzumab bind too and what does is cause?

A

The ErbB2/.ErbB3 complex disruption and casues Ligand- INdependent signaling (AKT & PI3 activation)

123
Q

What does Pertuxumab bind too and what does it cause?

A

Binds to ErbB2 ErbB1/3/4 complex adn causes Inhibiton of Lignad-Dependent signaling

124
Q

What does Iapatinib bind too adn what does it cause?

A

binds to ErbB2 ErbB1/3/4 and causes inhibiton of Ligand-dependent adn Ligand- independent signaling (inhibiton of ErbB1/2 TK activity)

125
Q

What is rituximab’s mechanisms of cytotoxicity?

A

directly
ADCC
Complment activation

126
Q

Drug:

Gemtuzumab

A

Mechanism:
apoptosis, ADCC
EGFR-2 Her-2/neu

127
Q

Drug: Trastuzumab

A

Mechanism:
Aoptosis, ADCC
EGFR-2 Her-2/neu

128
Q

Drug: Cetuximab

A

mechanism:
Apoptosis, ADCC
EGRF-1, Her-1

129
Q

Drug: Panitumumab

A

mechanism:
Apoptosis, ADCC
EGRF-1, Her-1

130
Q

Drug: Bevacizumab

A

Mechanism; anti-angiogenesis, neovascularization VEFG BLOCK

131
Q

Drug: Rituximab

A

Mechanism
apoptosis, ADCC, CDC
CD-20 targeted

132
Q

Drug Ofatumumab

A

Mechanism
Aoptosis, ADCC, CDC
CD-20 targeted

133
Q

Alemtuxumab

A

mechanism:
Apoptosis, ADCC, CDC
CD-52 targeted

134
Q

Ibritumomab Tiuxetan

A

Mechanism:
Apooposis, weak phagocytosis, irradiation
CD-20targted

135
Q

Tositumomab

A

Mechanism: Apoptosism, ADCC, CDC, irradiation

CD-20 targeted

136
Q

That are the EGFR TKIs?

A

Gefitinib, Erlotinib (ErbB1, HER-1)

Lapatinib (ErbB1, HER-1 & ErbB2, HER-2)– has QT prolongation

137
Q

What are the BCR-ABL TKIs?

A

Imatinib adn Dasatinib

Nilotinib– QT prolongation

138
Q

What are the mechanisms of resistance to oral TKI?

A

decreased intracellular drug levels
increased plasma protein binding
MDR-1 (p-gp) mediated efflux
genomic amplification of kinase
clonal evolutiono f kinase-independent mechanism
mutation of ATP-binding site affecting drug binding or kinase activity (highly conserved site)

139
Q

What are the VEGF TKIs?

A

Sunitinib, Sorafenib, pazotanib– prolonged QT interval

140
Q

What are the mTORS?

A

sirolimus
everolimus
temsirolims

141
Q

What are the interferons?

A

casue muscle ache and fever

interferon-alpha-2a, promote cell cycel arrest in Go, induces apoptosis induces immunological respone (CTLs and NK)

142
Q

What is Bortexomib’s pathway?

A

works on the NEMO pathway to prevent removal of IKB so NFkB cant activate cytokines

143
Q

What are the 3 factors influencing chemotherapeutic responses?

A

1) pharacokinetics
2) tumor-cell specific
3) tumor microenviornment

144
Q

What are the possible resistance mechanisms?

A

Antineoplastic Agent
1) decreased uptake of drug into cancer cell
2) failure to be metabolixed into pharmacologically active moiety
3)Enhanced metabolism to inactive products
4) Increased active transport of drug out of cancer cell
DNA, Target Enzyme, or othe rMacromolecule
1) repair of drug-induced DNA damage
2) gene amplification or increase gene transcription leading to an increased amount of target enzyme with in the cancer cell
3) reduced ability of drug to bind to target enxyme
4) increased levels of sulfhydryl scavengetrs
5) altered concentration of target proteins
6) increased expressionon antiapoptotic genes like bcl-2

145
Q

Oncology agent:

1) tumor lysis syndrome

A

Concurrent Agent:
1) Allopurinol, Rasburicase
to reduce uric acid level,; renal protective

146
Q

Oncology agent:

2) cyclophosphamide, ifosfamide

A

Concurrent Agent:

2) Mesna (protective against acrolein product)

147
Q

Oncology Agent: Cisplatin

A

Concurrent Agent: Amifostine (cytoprotection)

148
Q

Oncology Agent: MTX

A

Concurrent Agent: Leucovorin (metabolic resuce)

149
Q

Oncology Agent: 5-FU

A

Concurrent Agent: Leucovorin (enhanced action)

150
Q

Oncology Agent: 6-MP

A

Concurrent agent: Allopuniol (CAUTION: INCREASES TOXICITY!!!!!)

151
Q

Oncology agent: Antracyclines

A

Concurrently Agent:Dexroxazone (Fe chelator; reduced cardiotoxicity)

152
Q

Oncology agent: Bone metastases

A

Concurrent agent: pamidronate, zoledronate (reduced bone pain and fractures)

153
Q

What drugs are shoulw to have CV morbidity (CHF and LV dysfunction)?

A

Anthracyclines adn Mitoxantrone

154
Q

What causes Hypertension?

A

Bevacizumab, sorafenib, sunitinib

155
Q

What causes edema

156
Q

What causes QT prolongation or TP?

A

Sorafenib, Sunitinib

157
Q

What casues thrombo-embolic complications?

A

Bevacizumab, Thalidomide, Estramustine

158
Q

What are the substrates for energy dependent efflux pumps?

A 
cisplatin
boxorubicin
daunorubicin
etoposide
paciltaxel
teniposide
topotecan 
vinblastine

Pharmacology (3 decks)

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