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Oncology > Oncology Meds > Flashcards

Oncology Meds Flashcards

1
Q

MOA of fluoridated pyrimidines:
Fluorouracil (Adrucil)
Capecitabine (Xeloda)
Trifluridine/Tipiracil (TAS-102, Lonsurf)

A

Once phosphorylated to active forms, 5-FU:
Gets incorporated into RNA as a false base, interfering with its function.
Gets incorporated into DNA, causing destabilization.
Inhibits thymidylate synthase, reducing available bases for DNA and RNA synthesis.

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2
Q

5-FU (Adrucil) is used in which disease states?

A 
Colorectal cancer
Breast cancer
Gastric cancer
Pancreatic cancer
Head and neck cancer
Ovarian cancer
Skin cancer (topical)
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3
Q

Adrucil cause which ADRs?

A 
Mucositis 
Diarrhea
Hand-foot syndrome
Myelosuppression (9-14 days)
N/V
Hyperpigmentation
Photo sensitivity
Ocular toxicity
Myocardial ischemic symptoms
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4
Q

Monitoring for 5-FU:

A

CBC
Stool count
Hands and feet for early signs of skin breakdown

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5
Q

What happens in a patient with DPD (dihydropyrimidine dehydrogenase, an enzyme involved in the metabolism of uracil and thymine) deficiency?

A

DPD deficiency = increased toxicity

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6
Q

What disease does capecitabine (Xeloda) treat?

A

Colorectal cancer

Breast cancer

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7
Q

ADRs associated with Xeloda are?

A

Diarrhea
Hand-foot syndrome
Mild N/V

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8
Q

What should be monitored when a patient is taking Xeloda?

A

Stool count

Hands and feet for early signs of skin breakdown

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9
Q

What is the drug interaction between capecitabine and warfarin?

A

Increase in INR

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10
Q

Which cancer is treated with trifluridine/tipiracil (Lonsurf)?

A

Colorectal cancer

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11
Q

ADRs caused by Lonsurf?

A

Myelosuppression
Decreased in appetite
N/V/D

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12
Q

Monitoring with Lonsurf?

A

CBC

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13
Q

MOA of leucovorin and it’s indications?

A

Stabilize binding of 5-FU to thymidylate synthase, prolonging the cytotoxic effect. Also repletes stores of reduced folates, overcoming methotrexate inhibition of folate cycle and reducing toxicity.

Indicated:
Colorectal cancer, in combo with 5-FU
Leucovorin rescue after high dose methotrexate

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14
Q

What is the MOA of cytarabine (Ara-C, Cytosar-U) and gemcitabine (Gemzar)?

A

When converted to tri-phosphate forms, competitively inhibit DNA polymerase, halting chain elongation.
Also gets incorporated into DNA as a false base, interfering with replication and transcription.

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15
Q

What is the MOA of the cytarabine analogs Azacitidine (Vidaza) and Decitabine (Dacogen)?

A

Gets incorporated into DNA, inhibiting DNA methyltransferase, causing hypomethylation of DNA.
Hypomethylation exposes genes for transcription, including genes responsible for differentiation and apoptosis.

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16
Q

Cytarabine (Ara-C) is used to treat which cancer?

A

Leukemias (AML, CML, ALL)

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17
Q

ADRs of Ara-C are?

A 
Myelosuppression (7-10 days)
N/V/D
Mucositis
Tumor lysis syndrome
Flu-like syndrome
Rash
High dose Ara-C (HiDAC):
Cerebellar toxicity 
Conjunctivitis
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18
Q

Monitoring for Ara-C include?

A

CBC
Signs of infection
Renal function
Signs of confusion due to cerebellar toxicity

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19
Q

What is a pearl for Ara-C use?

A

Dexamethasone eye drops must be administered with HiDAC to prevent conjunctivitis

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20
Q

In which cancer is gemcitabine (Gemzar) used?

A 
Pancreatic
Lung
Breast
Ovarian
Bladder
Soft tissue sarcomas
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21
Q

ADRs caused by Gemzar are?

A 
Myelosuppression (10-14 days)
Flu-like syndrome
Rash
Elevation in liver transaminases
N/V
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22
Q

Monitoring for gemcitabine include?

A

CBC

LFTs

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23
Q

Azacitidine (Vidaza) treats:

A

MDS

AML (not FDA approved)

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24
Q

ADRs of Vidaza and Dacogen are:

A 
Myelosuppression (10-17 days)
Infection
Musculoskeletal symptoms (arthralgias)
Cough
Dyspnea
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25
Q

What is the MOA of mercaptopurine (6-MP, Purinethol)and thioguanine (6-TG, Tabloid)?

A

They are structural analogs of guanine that undergo conversion by hypoxanthine guanine-phosphoribosyltransferase and are incorporated into DNA and inhibit purine nucleotide synthesis.

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26
Q

What is the MOA of fludarabine (Fludara) and clofarabine (Clolar)?

A

They are triphosphate derivatives that inhibit ribonucleotide reductase and are incorporated into DNA and RNA.

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27
Q

What is the MOA of cladribine (Clolar) and pentostatin (Nipent)?

A

They inhibit adenosine deaminase, interfering with adenosine nucleotide synthesis.

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28
Q

6-MP is used to treat:

A

AML
ALL
CML

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29
Q

ADRs caused by 6-MP are:

A 
Myelosuppression (7-10 days)
Dry skin
Rash
Photo sensitivity
Hepatoxicity
Jaundice 
Hyperbilirubinemia
N/V
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30
Q

Pearls for 6-MP are:

A

Dose reduction is required if co-admin with allopurinol

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31
Q

6-TG is used to treat:

A

AML

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32
Q

ADRs for 6-thioguanine are:

A 
Myelosuppression (7-10 days)
Increased LFTs
Mucositis
Rash
N/V
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33
Q

Fludarabine is used in which disease states?

A

Hairy cell leukemia
CLL
AML
Follicular lymphoma

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34
Q

ADRs caused by fludarabine are:

A 
Myelosuppression (10-14 days), including decreased T cells
Diarrhea
CNS toxicity (rare)
Somnolence
Peripheral neuropathies
Hearing and visual changes
AMS
Seizures, pulmonary toxicity, TLS
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35
Q

Clofarabine is used to treat:

A

AML

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36
Q

ADRs caused by clofarabine are:

A 
Myelosuppression (7-9 days)
N/V/D
Hypokalemia
Hypophosphatemia
Cytokine release syndrome
Increased hepatic enzymes
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37
Q

Cladribine is used to treat:

A 
Hairy cell leukemia
CLL
CML
Mantle cell lymphoma
Non-Hodgkin’s lymphoma
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38
Q

ADRs caused by cladribine are:

A

Myelosuppression (5-10 days)
Fever (onset by day 6, persisting for about 3 days)
Immunosuppressive
Severe opportunistic infections

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39
Q

Pearls for fludarabine, clofarabine, cladribine:

A

Prophylactic antibiotics and antiviral meds are recommended due to long-lasting T-cell suppression

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40
Q

MOA of antifolates such as methotrexate (Folex, MTX), pralatrexate (Fotolyn), and pemetrexate (Alimta)?

A

MTX inhibits DHFR, the enzyme responsible for reducing dihydrofolate to tetrahydrofolate for the production of dTMP from dUMP.
This results in the depletion of intracellular pools of reduced folates essential for thymidylate and purine synthesis.
The DHFR-mediated effects of antifolates on normal and tumor cells may be neutralized by supplying reduced folates exogenously.
The reduced folate used clinically for ‘’rescue’’ is leucovorin (folinic acid), which bypasses the metabolic block induced by DHFR inhibitors.

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41
Q

MTX is used in which types of cancer?

A 
ALL
Non-Hodgkin’s lymphoma
Sarcomas
Breast
Head and neck
Lung
Stomach
Esophagus
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42
Q

ADRs caused by MTX are:

A 
Myelosuppression (~10 days)
Mucositis
Renal dysfunction at high doses
N/V
CNS toxicity (more severe with IT administration)
Hepatoxicty
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43
Q

Monitoring for MTX consists of:

A 
CBC
LFTs
Renal function
Urine pH
MTX drug levels with high dose
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44
Q

Pearls for MTX

A

3rd spaces (ascites, edema, plural effusion)
Can have long T1/2, may require prolonged leucovorin rescue
Drugs that are highly protein bound may displace MTX from albumin and increase toxicity (sulfonamides, salicylates, phenytoin, tetracyclines)
NSAIDs and PPIs compete for renal excretion of MTX and increase serum drug levels

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45
Q

Which disease states is pralatrexate (Folotyn) used?

A

Peripheral T-cell lymphoma

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46
Q

ADRs caused by Folotyn?

A 
Myelosuppression 
Mucositis
N/V/V
Anemia
Fatigue 
Edema
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47
Q

Which disease state dose Alimta treat?

A

Mesothelioma
NSCLC
Ovarian cancer (not FDA approved)

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48
Q

ADRs for Alimta:

A 
Myelosuppression (8-10 days)
Stomatitis
Pharyngitis 
Rash
Desquamation
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49
Q

Pearls for Alimta and Folotyn are:

A

Begin oral folic acid supplementation 10 days prior to intimacy dose and continue for 30 days after last dose

Vitamin B12 IM injection within 10 weeks prior to initial dose and every 8-10 weeks thereafter

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50
Q

MOA of glucarpidase (Voraxaze):

A

It is a recombinant form of the bacterial enzyme carboxypeptidase-G2. It hydrolyzes the carboxyl-terminal glutamate residue from extra cellular methotrexate into inactive metabolites (DAMPA and glutamate). Allows for rapid reduction of methotrexate concentrations independent of renal function.

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51
Q

What is the indication for glucarpidase (Voraxaze)?

A

Methotrexate toxicity with MTX concentration > 1 mcg/L when leucovorin rescue alone is insufficient.

Can be used off-labeled for IT MTX toxicity.

Very expensive

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52
Q

What is the MOA of vinca alkaloids, eribulin, and Estramustine?

A

They are micro assembly inhibitors. They prevent formulation and induce destabilization of microtubules.

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53
Q

What is the MOA of taxanes and Ixabepilone?

A

They are microtubule disassembly inhibitors. They work by stabilizing microtubules.

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54
Q

What is the more precise MOA of vincristine (Oncovin), vinblastine (Velban), and vinorelbine (Navelbine)?

A

Vinca alkaloids bind to tubulin alpha and beta subunits, inhibiting polymerization into mitotic spindles during metaphase.

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55
Q

Oncovin is used in which disease states?

A 
Leukemia
Hodgkin’s and non-Hodgkin’s lymphoma
Neuroblastoma
Rhabdomyosarcoma
Ewing’s sarcoma
Wilms’ tumor
Multiple myeloma 
Thyroid and brain tumors
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56
Q

ADRs caused by Oncovin are:

A

Peripheral neuropathy
Motor sensory, autonomic, and cranial nerves may be affected (paresthesias, ileus, urinary retention, facial palsies) - irreversible
SIADH
Myelosuppression

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57
Q

Monitoring for Oncovin include:

A

Signs of neurotoxicity (tingling in extremities,constipation.CNS toxicity)
LFTs

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58
Q

Pearls for vinca alkaloids:

A

NEVER ADMIN INTRATHECALLY
Inject hyaluronidase intradermally and apply moderate heat for extravasation.
Doses should be adjusted in pts with elevated bilirubin
Prevent ileus by treating constipation aggressively.
Vincristine doses capped at 2 mg to minimize neurotoxicity.

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59
Q

Which disease states does vinblastine (Velban) treat?

A 
Hodgkin’s and non-hodgkin’s 
T-cell lymphoma
Testicular
Breast
Lung
Head and neck
Bladder
Kaposi’s sarcoma
Choriocarcinoma
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60
Q

ADRs caused by Velban are:

A 
Myelosuppression (5-10 days)
Mucositis
Neurotoxicity - less common than Oncovin
Myalgias
SIADH (rare)
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61
Q

Which disease states does vinorelbine (Navelbine) treat?

A

NSCLC
Breast
Ovarian
Hodgkin’s disease

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62
Q

ADRs caused by Navelbine are:

A 
Myelosuppression (5-10 days)
Mucositis
Neurotoxicity- less common than Oncovin
Myalgias
SIADH (rare)
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63
Q

What is the MOA of taxanes?

A

Bind temporarily to low-affinity sites on the exterior of the microtuble and later migrate to high-affinity sites within the lumen. Promote assembly of microtubules from tubulin diners and stabilize microtubules by preventing depolymerization.
Induce abnormal arrays or ‘’bundles’’ of microtubules throughout the cell cycle and during mitosis.

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64
Q

Which disease states does paclitaxel (Taxol) treat?

A 
Breast
Ovarian
NSCLC
Cervical
Prostate
Testicular
Others
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65
Q

ADRs caused by Taxol are:

A 
Myelosuppression (10-12 days)
Infection
Hypersensitivity reactions
Peripheral neuropathy 
Myalgias or arthralgias
Mucositis
Cardiac arrhythmia
Alone is
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66
Q

Pearls for Taxol are:

A

Premed with steroids and antihistamines

Admin BEFORE platinums

Dose reduction in pts with hepatic impairment

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67
Q

Which disease states is treated with nab-paclitaxel (Abraxane)?

A

Breast
NSCLC
Pancreatic cancer

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68
Q

ADRs caused by nab–paclitaxel (Abraxane) are?

A 
Myelosuppression (10-12 days)
Infection
Peripheral neuropathy 
Myalgias or arthralgias 
Mucositis
Cardiac arrhythmias
Slope is
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69
Q

Pearls for Abraxane are:

A

This formulation lack Camaphor solvent which is responsible for hypersensitivity reactions

NOT interchangeable with paclitaxel

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70
Q

Which disease states does docetaxel (Taxotere) treat?

A 
Breast
NSCLC
Stomach
Head and neck
Prostate
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71
Q

ADRs caused by docetaxel are:

A 
Myelosuppression (5-9 days)
Fluid retention and edema
Pleural effusions
Ascites
Alopecia
Rash
Peripheral neuropathy 
Hypersensitivity reactions
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72
Q

Pearls for docetaxel are:

A

Premed with dexamethasone x 3 days, beginning day before chemo

CI in pts with hepatic impairment

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73
Q

Disease state that is treated with cabazitaxel (Jevtana) is?

A

Prostate cancer

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74
Q

ADRs caused by cabazitaxel (Jevtana) are:

A 
Myelosuppression (8-12 days)
Infection
Hypersensitivity reactions
N/V/D
Asthenia
Renal failure
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75
Q

Pearls for Jevtana are:

A

Premed with steroids and antihistamines

Avoid in pts with hepatic impairment

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76
Q

What is the MOA of Ixabepilone (Ixempra)?

A

Binds to the beta-tubulin subunit of the microtubule, stabilizing tubulin polymerization and stabilizing microtubular function.
Arrests cell cycle at the G2/M phase and induces apoptosis.

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77
Q

Which type of cancer does Ixabepilone (ixempra) treat?

A

Breast

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78
Q

ADRs caused by Ixempra are?

A 
Myelosuppression
Peripheral neuropathies
Hypersensitivity reactions
Asthenia
Arthralgias
Alopecia
79
Q

Pearls for Ixempra are:

A

Premed with steroids and antihistamines

Dose reduce in pts with hepatic impairment

80
Q

MOA of eribulin (Halaven):

A

Binds to high affinity sites at the ends of existing microtubules.
Inhibits formation of mitotic spindles causing mitotic breakage and arresting the cell cycle at the G2/M phase.

81
Q

Disease state in which eribulin (Halaven) is used?

A

Breast

82
Q

ADRs of eribulin:

A 
Myelosuppression (~day 13)
Peripheral neuropathies 
Asthenia
Alopecia
N/C
83
Q

Pearls for eribulin:

A

Dose reduce in pts with hepatic impairment

May cause QT prolongation

84
Q

MOA of Estramustine (Emcyt):

A

Estradiol suppresses circulating levels of testosterone.
Estramustine binds covalently to microtubule-associated proteins that are part of the structural support for microtubules.
Causes separation of these proteins from microtubules, inhibiting microtubule assembly and eventually causing disassembly.

85
Q

Which disease state does Estramustine (Emcyt) treat?

A

Prostate

86
Q

ADRs of Emcyt:

A

Estrogenic side effects (breast tenderness/enlargement, edema)
Increase in LFTs
N/D

87
Q

MOA of topoisomerase inhibitors is:

A

Topoisomerases are essential enzymes involved in maintaining DNA topological structure during replication and transcription.
DNA topoisomerase enzymes relieve torsional strain during DNA unwinding by producing strand breaks.
Topoisomerase I produces single strand breaks; topo II produces double strand breaks

88
Q

MOA of irinotecan (Camptosar), irinotecan liposomal (Onivyde), and topo Texan (Hycamptin)?

A

Inhibit topo I resulting in the stabilization of the ‘’cleavable complexes’’ causing reversible single-stranded breaks.

89
Q

Which disease states does irinotecan treat?

A

Colorectal

Pancreatic

90
Q

ADRs caused by irinotecan are:

A 
N/V/D
Myelosuppression 
Alopecia
Fatigue
Increased LFTs
Pulmonary toxicity 
Diffused infiltrates
Fever 
Dyspnea
91
Q

Pearls for irinotecan:

A

Diarrhea:
Early (24 h): atropine
Late (>24 h): loperamide

Use in caution in pts with hepatic impairment or UGT1A deficiency

92
Q

Which disease states does topotecan treat?

A

Ovarian
Cervical
SCLC

93
Q

ADRs caused by topotecan are:

A

Myelosuppression (8-11 days)
Mucositis
Reversible elevations in transaminases
Less N/D than irinotecan

94
Q

Pearls for topotecan are:

A

Dose reduction for renal impairment

95
Q

MOA of etoposide (Vepesid, Toposar) and Teniposide (Vumon)?

A

They stabilize ‘’cleavable complex” (topo II with the DNA strand cut) allowing DNA complex to break down leaving a double strand break.
The strand breaks are capped by remnants of the topoisomerase protein, making them difficult to repair. They arrest cells in the S or early G2 phase. And also bind to tubulin and interfere with microtubule.

96
Q

Which disease states does etoposide treat?

A 
SCLC
Testicular 
ALL
AML
Adrenal carcinoma
97
Q

ADRs of etoposide:

A 
Myelosuppression (7-14 days)
N/V
Alopecia
Mucositis 
Hypotension
Infusion-related and hypersensitivity reactions
98
Q

Pearls for etoposide and tenoposide:

A

May cause secondary malignancies such as leukemias.

99
Q

Disease states that tenoposide treat”

A

ALL

100
Q

ADRs of tenoposide:

A

Myelosuppression (7-10 days)
Mucositis
N/V/D

101
Q

MOA of doxorubicin (Adriamycin), liposomal doxorubicin (Doxil), daunarubicin (Cerubidine), idarubicin (Idamycin), and epirubicin (Ellence):

A

They induce formation of covalent DNA-topo II complexes, preventing re-ligation of DNA, causing strand breaks. Also intercalated between base pairs in the DNA, causing additional DNA strand breaks.
Metabolism of anthracyclines (but not mitoxandrone) forms oxygen free radicals that add to cytotoxicity.

102
Q

How is liposomal doxorubicin different from regular doxorubicin?

A

Liposomal encapsulation of the doxorubicin limits cardiotoxicity.

103
Q

Which disease states does adriamycin treat?

A 
Breast
Ovarian
Uterine
Bladder
Thyroid
Lymphomas
Leukemias
104
Q

ADRs of Adriamycin:

A 
Myelosuppression (10-14 days)
Infusion pain
Alopecia
Mucositis 
N/V
Radiation recall reactions
105
Q

Which disease state does Doxil treat?

A

AIDS-related Kaposi’s sarcoma
Breast
Ovarian

106
Q

ADRs of Doxil:

A 
Myelosuppression (10-14 days)
Hand-foot syndrome
Alopecia
N/V
Mucositis 
Fatigue
107
Q

Which disease states does daunorubucin treat?

A

AML

ALL

108
Q

ADRs of daunorubicin:

A 
Myelosuppression (10-14 days)
Mucositis 
N/V
Alopecia
Severe vesicant
109
Q

Disease states that idarubicin treat:

A

ALL
AML
CML
MDS

110
Q

Disease states that epirubicin treat:

A

Breast cancer

111
Q

Disease states that mitaxantrone (Novantron) treat:

A

Breast
Prostate
AML
NHL

112
Q

ADRs of idarubicin:

A 
Myelosuppression (10-15 days)
Mucositis 
N/V
Alopecia
Severe vesicant 
Cardiac toxicity
113
Q

ADRs of epirubicin:

A 
Myelosuppression (8-14 days)
Mucositis 
N/V
Alopecia
Severe vesicant injury
Cardiac toxicities
114
Q

ADRs of mitaxandrone:

A 
Myelosuppression (10-14 days)
N/V
Mucositis 
Alopecia 
Less cardiotoxic than the anthracyclines
115
Q

Pearls for anthracyclines (‘’rubicin’’, mitoaxandrone):

A

May discolor urine and sweat.
Extravasation: apply cold and infuse IV dexrazoxane.

Cardio toxicity (acute): not related to cumulative dose; arrhythmias, pericarditis 
Cardiac toxicity (chronic): cumulative injury to myocardium (total dose > 450-550 mg/m2 doxorubicin equivalents)
116
Q

What is the indication for dexrazoxane (Zinecard, Totect):

A

Prevention of doxorubicin cardiomyopathy.

Treatment of anthracycline extravasation

117
Q

MOA of dexrazoxane:

A

A potent intracellular chelating agent.

Cardiomyopathy: scavenges iron-mediated oxygen free radical generation responsible for anthracycline-induced cardiomyopathy.

Extravasation: reversibility inhibits topo II, protecting tissue from anthracycline cytotoxicity

118
Q

MOA of alkylating agents: cyclophosphamide, ifosfamide, bendamustine, mechlorethamine, melphalan, chlorambucil, carmustine, lomustine, busulfan, temozolamide, dacarbazine, and ethylenimines?

A

Covalently bind to highly reactive alkyl groups of nucleic acids and some proteins —> cross-linking.
Interstrand: between bases on opposite strands
Intrastate: between 2 bases in the same strand.
Greatest effect is seen in rapidly dividing cells.

119
Q

Disease states treated with cyclophosphamide (Cytoxan):

A 
Lymphoma (Hodgkin’s and NHL)
Breast 
SCLC
Leukemias
Multiple myeloma 
BMT
120
Q

ADRs of cyclophosphamide:

A 
Hemorrhagic cystitis
NV
Myelosuppression (10-14 days)
Alopecia
SIADH (doses >2 g/m2)
Secondary malignancies (bladder, acute leukemia)
Infertility, sterility
121
Q

Disease states treated with ifosfamide:

A 
Testicular 
Soft-tissue sarcomas
Lung
Breast
Ovarian
Bladder
Lymphomas
122
Q

ADRs of ifosfamide:

A 
Hemorrhagic cystitis 
Nephrotoxicity
Myelosuppression (10-14 days)
CNS effects (somnolence, confusion,disorientation, cerebellar symptoms that are dose-related
N/V -acute and delayed
123
Q

Pearls for cyclophosphamide (Cytoxan) and ifosfamide (Ifos):

A

Advise pts to drink lots of fluids (>3 liters/day).
Administer with mesna (all ifosfamide, high-dose cyclophosphamide).
Dose reduce for renal impairment>

124
Q

Indication for mesna (Mesnex):

A

Prophylaxis of hemorrhagic cystitis induced by ifosfamide or high dose cyclophosphamide.
Administered IV or PO prior to or along with chemo.

125
Q

MOA of mesna:

A

Acrolein: toxic metabolite of cyclophosphamide and ifosfamide.
Acrolein binds to sulhydryl groups in the bladder wall causing hematuria, urinary frequency and dysuria.
Mesna contains a free sulfhydryl group which binds acrolein excreted in the urine before it can bind to the bladder wall.

126
Q

Disease states treated by bendamustine (Treanda):

A

CLL

NHL

127
Q

Disease states treated by mechlorethamine (Mustargen):

A

Lymphomas (Hodgkin’s and NHL)
Cutaneous T-cell lymphoma
Breast
Lung

128
Q

ADRs of bendamustine (Treanda):

A 
Myelosuppression (14-21 days)
Infection
Dermatologic reactions including SJS
TLS
Infusion reactions
129
Q

ADRs of mechlorethamine (Mustargen):

A 
Myelosuppression (~14 days)
N/V/D
Alopecia 
Mucositis 
Taste changes
130
Q

Pearls for mechlorethamine:

A

Treat extravasation with sodium thiosulfate

131
Q

Disease states treated with melphalan (Alkeran):

A 
Multiple myeloma 
BMT
Neuroblastoma
Breast
Ovarian
132
Q

Disease states treated with chlorambucil (Leukeran):

A

CLL
Lymphomas (Hodgkin’s and NHL)
Ovarian
Breast

133
Q

ADRs for melphalan:

A 
Myelosuppression (8-10 days)
N/V/D
Mucositis 
Alopecia 
Arrhythmia 
Nephrotoxicity
134
Q

ADRs for chlorambucil:

A 
Myelosuppression (~14 days)
Increased LFTs 
Skin rash
Menstrual irregularities 
Pulmonary toxicity 
Risk of secondary malignancies 
Infertility and sterility
Teratogenic
135
Q

Pearls for chlorambucil?

A

Take on an empty stomach

136
Q

MOA for nitrosureas such as carmustine and lomustine:

A

These alkylate DNA through chloroethyl moeity.

Lipophilic —> able to cross BBB

137
Q

Disease states treated with carmustine:

A 
Brain tumors
Multiple myeloma 
Lymphomas (Hodgkin’s and NHL)
Melanoma
Lung
Colorectal
138
Q

Disease states treated with lomustine:

A 
Hodgkin’s 
Intracranial tumors
Breast
Colorectal lung
Multiple myeloma 
NHL
139
Q

ADRs of carmustine and lomustine:

A 
Myelosuppression (4-5 days)
Severe N/V
Cumulative nephrotoxicity 
Pulmonary fibrosis 
Facial flushing during infusion
140
Q

Pearls for lomustine:

A

Take on an empty stomach with fluids

141
Q

Disease states treated by busulfan:

A

CML
AML
BMT

142
Q

ADRs caused by busulfan:

A 
Myelosuppression (14-21 days)
Skin hyperpigmentation
Pulmonary fibrosis
Gynecomastia
Adrenal insufficiency 
High dispose toxicities: seizures,hepatic venoocclusive disease, severe N/V
143
Q

Pearls for busulfan:

A

Seizure prophylaxis with high doses

PK monitoring is required with IV busulfan

144
Q

MOA of temozolamide (Temodar) and dacarbazine:

A

Undergo demethylation to active intermediate monoethyl triazenoimidazolecarboxamide. Decomposes to methylcarbonium ion, a nucleophile which alkylates DNA at the O6 and N7 positions of purines.
Temozolamide is almost 100% orally absorbed can can cross the BBB. Dacarbazine does not cross the BBB.

145
Q

Disease states treated with temozolamide:

A

Brain tumors

146
Q

Disease states treated with darcarbazine:

A 
Melanoma
Hodgkin’s
Soft-tissue sarcomas
Neuroblastoma
Fibrosarcomas
Rhabdomyosarcoma
Thyroid cancer
147
Q

ADRs of temozolamide and darcarbazine:

A 
Myelosuppression (7-10 days)
Severe N/V
Increased liver enzymes
Flu-like syndrome
Flushing
Photosensitivity
148
Q

Temozolamide pearls:

A

Requires prophylaxis for PJP

149
Q

MOA of ethylenimines:

A

Release ethylenimines radicals that behave like nitrogen mustards

150
Q

Disease states treated by thiotepa (Thioplex):

A 
Leukemias
Hodgkin’s 
Breast
Ovarian
Bladder
BMT
151
Q

ADRs of thiotepa:

A 
Myelosuppression (7-10 days)
N/V
Mucositis 
Pruritus
Dermatitis
152
Q

Pearls for thiotepa:

A

May be excreted in sweat, be especially conscientious of skin care in high-dose regimens.

153
Q

MOA of platinums such as cisplatin, oxaliplatin, and carboplatin:

A

Platinum salts undergo Aquarian once inside the cell.
The platinum atom binds covalently to the N7 position to form inter and intra strand crosslinks.
Platinum-DNA adductor cause replication arrest, transcription inhibition, cell-cycle arrest, DNA repair and apoptosis.

154
Q

Disease states treated with cisplatin (Platinol):

A 
Testicular 
Ovarian
Bladder
Head and neck
Lung
Breast
Cervical
Gastric 
Colorectal
155
Q

Disease states treated with carboplatin:

A 
Ovarian
Breast
Lung
Head and neck
CNS or germ cell tumors
Osteogenic sarcomas
156
Q

Disease states treated with oxaliplatin:

A

Colorectal
GI
Breast

157
Q

ADRs of cisplatin:

A 
Severe N/V
Nephrotoxicity 
K and Mg wasting
Neurotoxicity 
Mild myelosuppression (14-23 days)
158
Q

ADRs of carboplatin:

A

Myelosuppression-thrombocytopenia (~21 days)
N/V -acute and delayed
Risk of hypersensitivity reactions at higher cumulative doses

159
Q

ADRs for oxaliplatin:

A

Peripheral neuropathy
Pharyngolaryngeal dysesthesias
N/V
Anaphylaxis risk

160
Q

Pearls for cisplatin:

A

Administer with pre and post hydration

161
Q

Pearls for carboplatin:

A

Dose per AUC not mg/m2

162
Q

Pearls for oxaliplatin:

A

Causes cold-induced neuropathy

163
Q

Calvert formula

A

Dose (mg) = Target AUC x (CrCl + 25)

Typical target AUC ranges from 2-7

Learn how to do this: IBW, ABW, or TBW?

164
Q

MOA of bleomycin (Blenoxane):

A

Intercalates at GC-rich portions of DNA.
Generates oxygen free radicals which produce single and double stranded DNA breaks.
Specific for G2 phase of cell cycle.

165
Q

MOA of mitomycin C (Mutamycin, MTC):

A

Alkylates DNA creating interstrand crosslinks and to a lesser extent also inhibits RNA and protein synthesis.

166
Q

Disease states treated with bleomycin:

A 
Testicular 
Lymphomas (HL and NHL)
Squamous cell cancers
Melanoma
Sarcoma
167
Q

Disease states treated with mitomycin:

A 
Stomach
Pancreatic
Anal
Bladder
Breast
Cervical
Colorectal
Head and neck
NSCLC
168
Q

ADRs of bleomycin:

A

Pulmonary fibrosis
Anaphylaxis and hypersensitivity reactions
Fever and flu-like symptoms
Mucositis

169
Q

ADRs of mitomycin:

A 
Myelosuppression (4-6 days)
Mucositis 
N/V
Vesicant
Pulmonary fibrosis
Hemolytic anemia
Uremic syndrome
170
Q

Pearls for bleomycin:

A

Pulmonary toxicity associated with cumulative dose >400 units and preexisting pulmonary disease and with concomitant use of G-CSF use.

171
Q

Pearls for mitomycin:

A

Apply ice or cold packs to site for extravasation

172
Q

MOA of hydroxyurea (Hydrea, Hydroxycarbamide)

A

Inhibits ribonucleotide reductase, preventing production of DNA nucleotides from RNA.

Cells accumulate in the S phase.

May be classified as an antimetabolite.

173
Q

Disease states of hydroxyurea:

A

Leukemias

174
Q

ADRs of hydroxyurea:

A 
Myelosuppression (~10 days)
Rash
Skin hyperpigmentation 
TLS
Secondary leukemias
175
Q

Pearls for hydroxyurea:

A

Used primarily to reduce WBC prior to standard chemotherapy.

176
Q

MOA of arsenic trioxide (Trisenox, ATO):

A

The precise mechanism of action of arsenic in acute promyelocytic leukemia (APL) remains to be clearly defined.
Selective apoptosis of APL cells mediated by activation of cysteine-proteases (caspases)
Induces damage and degradation of the fusion protein PML/RAR-alpha.
Upgrade the expression of NADPH-oxidase, leading to increase in production of reactive oxygen species.
Disrupts mitochondria transmembrane potential.

177
Q

Disease states treated by arsenic trioixide:

A

Acute promyelocytic leukemia (APL)

178
Q

ADRs of arsenic trioxide:

A

QT prolongation
Differentiation syndrome (pulmonary infiltrates, respiratory distress, fever, and hypotension)
Electrolyte abnormalities (hypo or hyperkalemia, hypomagnesemia)
Hyperglycemia
Rash, lightheaded ness, fatigue
Musculoskeletal pain

179
Q

Pearls for arsenic trioxide:

A

Differentiation syndrome must be treated promptly with corticosteroids

Do not give if QTc > 500 msec

Replace electrolytes before therapy

180
Q

MOA of retiniods, tretinoin (ATRA), alitretinoin, bexarotene:

A

Direct cell differentiation by binding to retinoid and retinoic acids receptors.

In APL, prompt leukemic cells to differentiate and cause apoptosis.

181
Q

Disease states treated with tretinoin (ATRA):

A

APL

182
Q

Disease state treated by alitretinoin (Panretin):

A

Kaposi’s sarcoma

183
Q

Disease states treated by bexarotene (Tegretin):

A

Cutaneous T-cell lymphoma

184
Q

ADRs tretinoin:

A 
Headache
Differentiation syndrome 
‘’ATRA syndrome’’: consisting of pulmonary symptoms, fever, hypotension, and pleural effusions
Dry skin and mucous membranes
Mucositis 
Elevation in transaminases and bilirubin
185
Q

ADRs of alitretinoin:

A

Rash

Itching

186
Q

ADRs of bexarotene:

A 
Increase TG and cholesterol 
Peripheral edema
Insomnia
Headache
Fever 
Hypothyroidism
Leukopenia
Anemia
187
Q

Pearls in tretinoin:

A

Differentiation syndrome must be treated promptly with corticosteroids

Teratogenic

188
Q

MOA omacetaxine (Synribo):

A

Exact MOA is unknown.

Decreases protein production, including oncoproteins Bcr-Abl and Mcl-1

189
Q

MOA of trabectedin (Yondelis):

A

MOA is unknown.

Binds and alkylates DNA at the N2 position of guanine.

Interferes directly with transcription.

Generates DNA double-stranded breaks.

190
Q

Disease states treated:

A

CML

191
Q

Disease states treated by trabectedin:

A

Sarcomas

192
Q

ADRs of omacetaxine:

A 
Myelosuppression - thrombocytopenia (14-21 days)
Increased risk of hemorrhage
Anemia, neutropenia, lymphopenia 
N/D
Fatigue 
Asthenia
Injection site reaction
Pyrexia, infection, hyperglycemia
193
Q

ADRs of trabectedin:

A 
Myelosuppression (~14 days)
Increased liver enzymes
Anemia
N/V/C
Electrolyte disturbances
Fatigue 
Muscle and joint pain

Oncology (6 decks)

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