SET3 Flashcards

1
Q

A patient with hepatic mets is slated to receive docetaxel as part of the therapy, what is a potential problem here?

A

Docetaxel (and other taxanes) are hepatically metabolized, so patients with bilirubin >7 due to infiltrative dz should have this held

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2
Q

What is the MOA of Fludarabine? AE?

A

Purine analog that inhibits DNA synthesis by interfering with DNA polymerase and Ribonucleotide reductase; lymphopenia and AIHA

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3
Q

What drugs are safe to give to pregnant woman with breast CA? When can you do it?

A

Cyclophosphamide and Doxorubicin in 2nd and 3rd trimester; Trastuzumab and Paclitaxel are not safe to give; trastuzumab can cause oligohydramnios

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4
Q

What drug should be given to HBV+ patients who are slated to begin Rituximab i.e. R-CHOP for DLBCL

A

Entacavir > Lamivudine

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5
Q

What drugs have been shown to be beneficial for prevention of chemotherapy-related neuropathy? Which for the treatment?

A

None shown to be beneficial in preventing but Duloxetine can treat chemo related peripheral neuropathy

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6
Q

If a person is to develop MDS or AML after exposure to Etoposide, when will it likely happen? What will be the abnormality?

A

2-3 years; 11q23 mutation affecting the MLL gene (Mixed Lineage Leukemia)

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7
Q

Where is CD52 found?

A

Mature lymphocytes; Alemtuzumab is anti-CD52 used in CLL but note that CD52 is on BOTH B and T lymphocytes so causes impaired cell-mediated immunity

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8
Q

What prophylaxis do patients receiving purine analogs (Fludarabine) or Alemtuzumab for CLL need?

A

Bactrim ppx because these drugs will cause lymphopenia not only of the B cells but also of T cells

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9
Q

What is the difference between paclitaxel and Nab-Paclitaxel?

A

Nab = nanoparticle albumin bound; it is a solvent free paclitaxel formulation that decreases solvent related reactions

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10
Q

Name 4 Microtubule destabilizing agents that prevent polymerization

A

Vinca Alkaloids (Vinblastine, Vincristine, Vinorelbine) and Eribulin (not vinca alkaloid)

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11
Q

What are the main adverse effects of TDM-1 (Kadcycla)?

A

Thrombocytopenia, increased LFT, cardiotoxicity (contains trastuzumab)

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12
Q

Why is subcortical edema commonly seen in PRES? Name 3 drugs that can cause it

A

The HTN and vasospasm lead to breakdown of BBB and hence edema leading to cortical blindness; Tacrolimus, Cyclosporine, and Bevacizumab

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13
Q

What is the MOA of taxanes? Name the 2 MC

A

They promote tubulin assembly into microtubles and inhibit their DEPOLYMERIZATION; paclitaxel and docetaxel

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14
Q

How long can hypomethylating agents such as azacitadine and decitabine take to show response?

A

Sometimes as long as 4-6 cycles; therefore would not consider the dz refractory after only a couple of cycles

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15
Q

What chemo drugs are vesicants? Which are irritants?

A

Vesicants = anthracyclines, vinca alkaloids; Irritants = taxanes and platinum analogs

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16
Q

Name 3 Vinca Alkaloids and their MOA

A

Vincristine, Vinblastine, Vinorelbine; Microtubule destabilizing agents that prevent polymerization

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17
Q

What are some adverse effects of Bevacizumab?

A

HTN is MC and basically is expected/on-target; organ perforation, PRES, nephrotic syndrome, DVTs, and poor wound healing

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18
Q

A patient with Her2+ breast CA that has received Cyclophosphamide + doxorubicin with weekly paclitaxel and is now on Trastuzumab and progressing could receive what?

A

Kadcycla (TDM-1) which is Trastuzumab + linker protein + maytansine and used in pt who have failed trastuzumab

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19
Q

True or False: An elderly pt with AML who is on decitabine has completed 2 cycles, her CBC is unchanged from baseline– she has refractory dz

A

False; hypomethylating agents such as 5-Azacitidine and Decitabine can take up to 4-6 cycles to show response

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20
Q

How long after allogeneic stem cell transplant should a person stay on posaconazole? How long should they have CMV monitored?

A

75 days; monitor for 6 months

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21
Q

What are three HDAC inhbitors that can be used in Cutaneous T cell Lymphomas that have failed other therapy?

A

Romidepsin, Vorinostat, Rocilinostat

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22
Q

MOA of Sunitinib

A

Affects multiple TKIs including VEGF and is used in metastatic RCC, often causes HTN which predicts for good outcome

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23
Q

What is the difference between Bevacizumab and ziv-aflibercept?

A

Bevacizumab targets VEGF-A; ziv-aflibercept targets VEGF-Trap

24
Q

What is the best antifungal for neutropenic ppx? How is it metabolized?

A

Posaconazole; hepatically

25
Q

What is the most concerning AE of Enzalutamide (i.e. for prostate CA)?

A

It can cause seizures, if this happens need to permanently stop the drug

26
Q

In AlloHSCT what are the MC infxns before engraftment occurs? From day engraftment to day 100?

A

Initially it is bacterial, viral, and fungal; from engraftment to day 100 CMV and fungal, so will be on posaconazole and monitor CMV until 6 months out from xplant

27
Q

What is the most serious AE of G-CSF?

A

Splenic rupture; more commonly bone pain

28
Q

What is an on-target side effect of drugs affecting the vascular endothelial growth factor pathway?

A

HTN i.e. Bevacizumab and Sunitinib

29
Q

What drug is a recombinant carboxypeptidase that converts MTX to glutamate?

A

Glucarpidase; used when high MTX levels and renal insufficiency

30
Q

A patient is slated to receive HD MTX for CNS ppx and is noted to have a moderate pulmonary effusion, next step?

A

Effusion needs to be drained as the MTX will sequester in the effusion and caused prolonged toxicity

31
Q

What is the MOA of Obinutuzumab?

A

It is a type II glycoengineered antibody that targets CD20

32
Q

What if you have given HD MTX to a person for CNS ppx and they happen to develop AKI for other reason and MTX level is elevated despite alkalinizing urine?

A

You can give Glucarpidase which is a recombinant carboxypeptide that converts MTX into glutamate

33
Q

What is another name for BCNU? Adverse effect?

A

Carmustine; delayed myelosuppresion i.e. up to 6w out from administration; 2nd line for GBM as first is surgery and temozolomide

34
Q

What is the other name for Kadcycla? What are the 3 components of it?

A

TDM-1; Trastuzumab + Linker Protein + Maytansine; Maytansine is inhibitor of tubulin polymerization; used for Her2+ metastatic Breast CA that progressed on trastuzumab and taxane

35
Q

What is the most common AE of aromatase inhibitors?

A

Arthralgias; also promotes osteoporosis, causes hot flashes

36
Q

For whom is Alemtuzumab approved? Explain why it can predispose to infxn?

A

CLL patients who have failed aklylating agents or fludarabine; CD52 expressed on both mature B and T lymphocytes so destroys both, loss of T cell = more infxn, monitor CMV q2 month

37
Q

What does Nab-Paclitaxel stand for? What is the brand name?

A

Nanoparticle Albumin Bound-Paclitaxel; Abraxane

38
Q

True or False: a history of alcohol use predicts for a patient to have a lot of adverse effects from chemo

A

False; in fact their CYP enzymes are on overdrive from the chronic EtOH consumption so they deal with chemo better

39
Q

Kehr sign may be seen when giving what supportive agent during chemo?

A

G-CSF (Neulasta, Neupogen); Kehr sign is L sided shoulder pain from splenic rupture; splenic rupture is a rare AE of G-CSF

40
Q

The CLL11 trial showed that which of the following is best: Chlorambucil alone, Chlorambucil + Obinutuzumab, Chlorambucil + Rituximab

A

Chlorambucil + Obinutuzumab is best; Both obinutuzumab and rituximab are anti-CD20

41
Q

What second line agent for GBMs is notorious for causing delayed myelosuppression i.e. 6 weeks or more

A

Carmustine (BCNU); first line is surgery + temozolomide

42
Q

True or False: Patients on Sunitinib for RCC who develop moderate HTN should stop the drug

A

False, it is expected that the drug will cause HTN and this predicts for a good outcome

43
Q

Studies have shown that trastuzumab given in pregnancy can cause this issue

A

Oligohydramnios

44
Q

What clinical setting is Glucarpidase used? MOA?

A

it is a recombinant carboxypeptide that converts methotrexate to glutamate; used in patients who have elevated MTX levels and renal dysfxn; goal MTX level <0.05

45
Q

AML with MLL gene rearrangements can occur after exposure to what chemotherapeutics? Mutation?

A

Etoposide (topoisomerase II inhibitors, also doxorubicin which is a topoisomerase II inhibitor); 11q23 cytogenetic abnormality

46
Q

What second generation 5 HT3 receptor antagonist is approved for both immediate and delayed nausea and vomiting?

A

Palonosetron; has half life of 40 hours

47
Q

What medication can counteract potential tissue necrosis of anthracycline extravasation?

A

Dexrazoxane

48
Q

What are the effects of DNA methylation and acetylation on DNA transcription?

A

Methylation silences genes so hypomethylating agents help undo that; acetylation promotes transcription so HDAC inhibitors help prevent de-acetylation

49
Q

What is the concern with giving methotrexate in the setting of an effusion (any)?

A

MTX will sequester the into the fluid and stay there, so patients will have prolonged exposure (increased AUC) and therefore toxicities

50
Q

Name 4 Microtubule Stabilizing agents (that prevent depolymerization)

A

Paclitaxel, Docetaxel, Nab-Paclitaxel, and Ixabepilone

51
Q

What is the toxic metabolite of cyclophosphamide? What is the MOA of Mesna?

A

Acrolein; Mesna donates a thiol group to acrolein to neutralize it

52
Q

What are some adverse effects of taxanes at toxic levels? How are they cleared?

A

Fluid retention, effusions and myelosuppression; hepatically cleared so careful if elevated bilirubin i.e. hepatic met

53
Q

What two enzymes are affected by methotrexate? What other one is affected by pemetrexed?

A

Dihydrofolate reductase and thymidylate synthase; glycinamide ribonucleotide formyltransferase

54
Q

Arthralgias are most commonly caused by what breast cancer drugs?

A

Aromatase Inhibitors such as anastrazole and lestrozole

55
Q

What is Abraxane?

A

Nab-Paclitaxel (Nanoparticle Albumin Bound Paclitaxel)

56
Q

What infection do you need to test for anytime you are considering starting rituximab?

A

HBV if either HbSAg or HBcAg is positive check viral load with PCR and start entacavir and refer to gastroenterology

57
Q

What is the MOA of HDAC inhibitors?

A

By inhibiting HDACs they promote acetylation of histones; histone acetylation releases histones from DNA making transcription easier so you can transcribe more tumor suppressor genes that have been silenced