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MALIGNANT HEME > SET2 > Flashcards

SET2 Flashcards

1
Q

What is the MOA of Ifosfamide?

A

Nitrogen mustard alkylating agent and given with Mesna (thiol donor) to prevent hemorrhagic cystitis just like cyclophosphamide

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2
Q

What are the main adverse effects of 6-MP

A

Myelosuppression and increased LFTs

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3
Q

True or False: Steroids can decrease the efficacy of Ipilimumab

A

False; so if someone gets an autoimmune issue can give steroids

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4
Q

Name 3 adverse effects of 5-FU

A

Severe myelosuppression, cardiotoxicity in the form of coronary vasospasm, and tear duct stenosis

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5
Q

What drug is known to cause a cold-sensitive neuropathy and even cold-sensitive laryngospasm? When does this occur?

A

Oxaliplatin; it can occur shortly after transfusion and is usually transient

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6
Q

What is the MOA of Ara-C (Arabinosylcytarabine)?

A

It is a PYRIMIDINE antimetabolite that inhibits DNA synthesis (S phase)

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7
Q

What anti-CD30 conjugate is approved for Hodgkin after relapse and in anaplastic large cell lymphoma after failure of at least 1 regimen?

A

Brentuximab vedotin

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8
Q

Deficiency in UGT1A1 in a patient being given Irinotecan can predispose to what problem?

A

Toxicity: prolonged myelosuppression

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9
Q

What should you be concerned for in pt being tx with R-CHOP who develops neuro Sx and MRI shows large non-enhancing lesion?

A

Progressive Multifocal Leukencephalopathy; Rituximab, Brentuximab, and Ofatumumab all cause reactivation of JC virus

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10
Q

How is methotrexate excreted?

A

Renally, and often need to alkalinize urine if giving high dose MTX

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11
Q

What drug is a prodrug of 5-FU that can be taken orally?

A

Capecitabine

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12
Q

Deficiency of what enzyme can lead to Irinotecan toxicity?

A

UGT1A1 which is an enzyme of the glucuronidation pathway; leads to prolonged myelosuppression

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13
Q

Why cant you use G-CSF to support neutropenia in Hodgkin pt receiving ABVD?

A

G-CSF increases Bleomycin Pulmonary toxicity

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14
Q

What is the dose limiting toxicity of bolus 5-FU?

A

Myelosuppression + Cardiotoxicity (vasospasm); additionally, when given in colon CA, there are better response rates to infusional dosing than bolus anyway

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15
Q

What HEENT complaint might a patient on 5-FU have?

A

They can get tear duct stenosis

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16
Q

Erlotinib, Gefitinib, and Afatinib are approved in what setting in lung cancer?

A

Stage IV lung cancer that harbor the exon 19 OR exon 21 EGFR mutations

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17
Q

Which interferon can be used in some melanoma patients?

A

Interferon-alpha-2b

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18
Q

What should you be concerned for in a patient with FOLFOX on warfarin?

A

The infusional 5-FU can decrease warfarin metabolism leading to supratherapeutic INR, switch to LMWH

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19
Q

Why is leucovorin able to “rescue” cells when given with HD MTX?

A

It gets converted to folic acid derivatives like tetrahydrofolate but does NOT need dihydrofolate reductase to do this; of note it, for some reason, does NOT rescue cancer cells

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20
Q

True or False: a rash in a patient on Erlotinib is a sign that you should stop the drug

A

False, it actually predicts a good response to therapy

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21
Q

If a patient with ovarian CA is receiving infusion of paclitaxel and carboplatin and has infusion rxn what is the likely culprit?

A

Paclitaxel; reaction to cremophor, slow the infusion

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22
Q

What are the main side effects of Ipilimumab?

A

Can exacerbate autoimmune phenomena

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23
Q

What are the drugs in MVAC what is a situation when this can be used?

A

A regimen used in muscle-invaseive bladder CA; MTX, VinBLASTINE, Doxorubicin, Cisplatin

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24
Q

What is radiation recall and what drugs can cause it?

A

Inflammatory reaction at site of prior radiation when certain chemo agents administered; Adriamycin, Paclitaxel, Docetaxel, Gemcitabine, Capecitabine

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25
Q

Which causes reversible cardiotoxicity anthracyclines or trasztuzumab?

A

Trasztuzumab so if the EF starts to drop (i.e. >16% of baseline) you should hold it and re-evaluate 4-8w

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26
Q

What is the terminal enzyme in the process of converting capecitabine to 5-FU

A

Thymidine phosphorylase

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27
Q

The CONFIRM study determined the optimal dose of Fulvestrant to be what?

A

500 mg was better than 250 mg

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28
Q

What drug, derived from the plant Cephalotaxus fortunei, inhibits the initial protein elongation step and is approved for chronic or acclerated phase CML resistant to two or more TKIs?

A

Omacetaxine mepesuccinate

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29
Q

When is Interferon-alfa-2b used in melanoma?

A

In patients with high risk of recurrence such as +SLNB or Breslow thickness > 4mm

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30
Q

What kind of drug is Docetaxel and what is its major adverse effect? How is it excreted?

A

Taxane that causes severe neutropenia and anemia (myelosuppression) and is excreted hepatically; do not give if bilirubin >7

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31
Q

What is XELOX?

A

Capecitabine + Oxaliplatin; no leucovorin

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32
Q

What are the adverse effects of Sunitinib (i.e. for RCC)?

A

HTN (an on-target effect), Hand-Foot syndrome, stomatitis, hypothyroidism, CHF, adrenal insufficiency

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33
Q

Name two cancer drugs that can cause HUS

A

Gemcitabine and Mitomycin C

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34
Q

True or false: Denosumab is noninferior to Zoledronic acid in delaying skeletal events in patients with advanced metastatic CA to bone or myeloma

A

True you can use either one, zoledronic acid more common though

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35
Q

Gemcitabine is a pyrimidine analog that is metabolized within cells to what active nucleoside forms? What is their intracellular effect?

A

Gemcitabine diphosphate: inhibits ribonucleotide synthesis; Gemcitabine triphosphate: competes to be incorporated into DNA and halts DNA synthesis

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36
Q

Fully explain the process by which Capecitabine is converted to 5-FU

A

Capecitabine converted to 5’-DFCR in liver by carboxylesterase; in the tissue the cytidine deaminase converts to 5’-DFUR and finally in the tumor cell THYIDINE PHOSPHORYLASE converts to 5-FU

37
Q

How is the use of leucovorin in FOLFOX different from its use when given with HD MTX?

A

In HD MTX it is “Leucovorin Rescue”; in FOLFOX it increases the intracellular pool of 5, 10, methylenetetrahydrofolate which further increases inhibition of thymidylate synthase

38
Q

True or False: Only cyclophosphamide causes hemorrhagic cystitis, ifosfamide does not

A

False, they both do and both should be given with Mesna

39
Q

What are the two mutations that can confer EGFR TKIs?

A

EGFR gene T790M mutation which is the most common cause; also the MET-protooncogene can serve as resistance mechanism in 20%

40
Q

Thymidilate synthase, dihydrofolate reductase, and glycinamide ribonucleotide formyltransferase are all inhibited by this drug

A

Pemetrexed

41
Q

What is a standard emetic ppx in patients on High Risk Emetic Chemo (3)

A

Palonosetron 0.25 mg IV + Dexamethasone 12 mg IV + Fosaprepitant 150 mg IV

42
Q

What mutation confers resistance to EGFR TKIs in 50% of patients who are resistant?

A

T790M in the EGFR gene

43
Q

Why can Ifosfamide (nitrogen mustard alkylating agent) lead to severe encephalopathy?

A

It’s breakdown product chloroacetylaldehyde can cause this issue

44
Q

What are the adverse effects of Tamoxifen?

A

Endometrial CA, Cataracts, Strokes, Hot Flashes, DVTs

45
Q

Which drug is truly an ER antagonist without ANY agonist activity

A

Fulvestrant

46
Q

In addition to producing radical oxygen species, anthracyclines also inhibit what enzyme?

A

Topoisomerase II

47
Q

What are some EGFR TKIs for lung CA (3)? What are two EGFR antibodies for colon CA?

A

Erlotinib, Gefitinib, and Afatinib; Cetuximab and Panitumumab

48
Q

What is the MOA of Fulvestrant and when is it used?

A

It is a total ER antagonist without any partial agonist fxn, it downregulates the estrogen receptor and is used in post-menopausal women with ER + breast CA that have had progression after prior endocrine therapy

49
Q

What kind of drug is Bosutinib?

A

A TKI used to tx CML; can cause diarrhea

50
Q

What is the active metabolite of Irinotecan?

A

SN-38; it is 1000x more potent than irinotecan

51
Q

How is Capecitabine excreted?

A

Renally; is GFR <30 do not give, if GFR is 30-50 then dose reduce by 25%

52
Q

What enzyme helps to detoxify Halogenated Pyrimidines (i.e. Fluoro-uracil), deficiencies of which can lead to toxicities?

A

Dihydropyridine Dehydrogenase

53
Q

What supportive agent can increase the risk of Bleomycin pulmonary toxicity and so should not be given with ABVD?

A

G-CSF (i.e. Neupogen, Neulasta)

54
Q

What are the two general ways to dose 5-FU in colon CA? Which is better and why?

A

Bolus or Infusional. The dose limiting toxicity of bolus 5-FU is myelosuppression and cardiotoxicity and also, there are better response rates to infusional so infusional is better.

55
Q

Name 3 cancer monoclonal Abs that can lead to reactivation of JC virus

A

Rituximab, Ofatumumab, and Brentuximab

56
Q

Why does paclitaxel often cause hypersensitivity reactions? What kind of reactions are there?

A

Due to the Cremophor vehicle. Can lead to sinus bradycardia so be careful if hx of ischemia or on AV nodal blocking drugs

57
Q

What are the best antidepressants to give when given with Tamoxifen?

A

Citalopram and Venlafaxine, don’t inhibit CYP2D6 which others do, leading to build up of endoxifen

58
Q

What is Temozolamide often used for? What ppx do they need and why?

A

Glioblastoma multiforme; Bactrim because it causes significant lymphopenia and can therefore get Pneumocystis pneumonia

59
Q

What does Brentuximab vedotin target?

A

CD30

60
Q

Discuss early and late diarrhea from Irinotecan (i.e. I ran to the can)

A

Early Diarrhea within 24 h is cholinergic mediated and responds to atropine; Late diarrhea is at least 24 h out and tx with loperamide and FQs

61
Q

How should you deal with dosage of 6-MP if allopurinol is being given?

A

Dose reduce by 50%

62
Q

Why do patients get infusion reactions to paclitaxel and how to you manage?

A

Due to the Cremophor and the tx is to slow the rate of infusion

63
Q

Deficiencies in what enzyme can lead to 5-FU toxicity

A

Dihydropyridine Dehydrogenase

64
Q

Name two conditions that Brentuximab vedotin can be used in

A

Hodgkin after relapse from autoHSCT or failure of at least 2 chemo options; anaplastic large cell lymphoma that is CD30+ after failure of one tx

65
Q

What study showed that LMWH is better than warfarin in cancer related anticoagulation?

A

CLOT study

66
Q

What kind of cardiotoxicity occurs with 5-FU? What method of dosing ameliorates this?

A

Coronary Vasospasm, not as bad if given infusionally

67
Q

During which part of the cell cycle does methotrexate act, MOA?

A

S phase cant make DNA or RNA; inhibits dihydrofolate reductase which is involved in tetrahydrofolate synthesis; by doing so thymidine can be made into purines

68
Q

What study showed that Fulvestrant 500 mg monthly had better PFS than 250 mg monthly

A

CONFIRM study

69
Q

What is the MOA of topotecan? How is it excreted?

A

It is a topoisomerase I inhibitor (can be used in metastatic ovarian CA, for example); renally

70
Q

Which EGFR inhibitor can only be given in k-ras wild type metastatic colon CA?

A

Cetuximab

71
Q

What three enzymes are inhibited by Pemetrexed

A

Thymidylate synthase, dihydrofolate reductase, and glycinamde ribonucleotide formyltransferase

72
Q

What is the main adverse effect of Bosutinib?

A

Diarrhea

73
Q

What kind of antibody is Ipilimumab?

A

Anti-CTLA4 (CTLA = Cytotoxic T Lymphocyte Associated protein)

74
Q

How is Irinotecan excreted?

A

Hepatic excretion; the active metabolite, SN-38, is glucuronidated so in pt with UGT1A1 def (Gilbert’s) it should not be given because it will cause prolonged myelosuppression

75
Q

Name the pyrimidines

A

Cytosine, Uracil, Thymine

76
Q

What are the oral and IV forms of neurokinin-1 antagonists?

A

PO = aprepitant; IV = fosaprepitant

77
Q

True or false: cisplatin and carboplatin are equally efficacious for bladder CA

A

False, they usually are but here you have to use CISPLATIN i.e. in MVAC

78
Q

What is SN-38?

A

This is the active metabolite of Irinotecan that actaully inhibits Topisomerase I and prevents DNA unwinding

79
Q

What is Omacetaxine mepesuccinate?

A

It is a drug approved for chronic or accelerated phase CML with resistance to two or more TKIs

80
Q

What tyrosine kinases does Imatinib inhibit in CML and GIST?

A

CML = BCR-ABL; GIST = c-kit (CD117)

81
Q

What is the MOA of Irinotecan?

A

It is a topoisomerase I inhibitor and so prevents DNA from unwinding; active metabolite is SN-38

82
Q

Why is it that Rituximab can lead to severe myelosuppression?

A

There is high CD20 expression in the BM

83
Q

What is CD117

A

Mast/Stem cell growth factor receptor (SCFR) which is also known as protooncogene c-kit; so expressed in mastocytosis and GIST where c-kit mutation is driver and Tx with imatinib

84
Q

What infusion, initally thought to decrease oxaliplatin related neuropathy in FOLFOX, has since been debunked?

A

Infusion of calcium and magnesium, has NOT been shown to reduce either cumulative neurotoxicity or acute neuropathy

85
Q

Which drug is an IgG2 fully humanized antibody to EGFR?

A

Panitumumab

86
Q

What drug is known to be increased by allopurinol? What is a regimen this is used in?

A

6-MP (6-mercaptopurine); POMP (6-MP, MTX, Vincristine, Prednisone) which is maintenance for Philadelphia negative ALL

87
Q

What are the adverse effects of capecitabine?

A

Hand-Foot syndrome, diarrhea, stomatitis, and neutropenia

88
Q

A patient with a melanoma that has been excised but has high risk of recurrence such as +SLNB or Breslow thickness > 4 mm can be tx with what agent?

A

IFN-alfa-2b; can cause fevers and psych issues

MALIGNANT HEME (12 decks)

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