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Oncology > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

AC-T

A

Adriamycin (Doxorubicin Hydrochloride)
Cyclophosphamide (Cytoxan)
Paclitaxel (Taxol)

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2
Q

aTEzolizumab

A

(TEcentriq)
CPI
MOA: PDL-1
MP: -itis
Uses: Lung, liver, NSCLC, SCLC

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3
Q

AZAcitidine

A

(vidAZA)
MOA: Antimetabolite/Demethylating leads to decreased methylation which leads to decreased growth. Also, second action is that it is similar structure to genes and gets taken up in DNA and Fucks up the DNA
AE: Myelosuppression, Moderate Emetic,
MP: LFTs, BMP, Cbc
Uses: AML, MDS

NB: often takes four cycles before cells normalize quicker —often have to transfuse
—nadir 10-17d

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4
Q

Bevacizumab

A

(Avastin)
MOA: VEGF inh (vascular endothelial growth factor). Decreases healing, angiogenesis, poor wound healing
NB: 4 Ps
Pressure (b/p)
Perforation (bowel perf)
Protein (urine protein)
Perfect skin (wound healing)

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5
Q

Bortezomib

A

(Velcade)
MOA: Proteasome inh leads to apoptosis
AE: Myelosuppression, herpes reactivation, decrease b/p, Diarrhea, Constipation, peripheral neuropathy
Nadir: 11 days

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6
Q

Brentuximab vedotin

A

(Adcetris)
MOA: Anti CD30, works as antimicrotubual?
MP: cbc
AE: neuropathy (DLT), pancytopenia, URI
Uses: Hodgkin Lymphoma

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7
Q

Capecitabine

A

(Xeloda)
MOA: prodrug 5fu. Blocks methylization
Oral—1-14 days, 21day cycle
AE: Diarrhea and PPE more likely than with IV, myelosuppression, mucositis, neuropathy,
MP: CBC, INR (if on VitK agonist, ie, Warfarin), Hydration, PPE
NB: Hep B screen, warnings if on warfarin,

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8
Q

Carboplatin

A

MOA: Alk agent,
MP: Delayed myelosuppression, (DLT) up to 3-4 wks, Oto/nephro toxic, incr LFTs.
NB: Dosing AUC using Cockroft-Gault for 0.8creatinine
NB: Cap GFR 125
Nadir: 21 days

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9
Q

Carfilzomib

A

(Kyprolis)
AE: Myelosuppression
Uses: Multiple Myeloma
NB: VTE ppx =/> 81mg ASA

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10
Q

CemipLImab

A

(LIbtayo)
CPI
MOA: Binds PD-1, blocking PD-L1 & PD-L2
Uses: BCC, SCC, Cervical Cancer, NSCLC.
MP: Itis
Generally 21 day cycles, IV, x 8cycles

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11
Q

CHOP

A

Cyclophosphamide (Cytoxan)
Doxorubicin Hydrochloride (Adriamycin)
Vincristine (Oncovin)
Prednisone

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12
Q

Cisplatin

A

MOA: Alk agent, platinum based
AE: nephrotic, N/V (DLT), ototoxic

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13
Q

CPI

A

Check point inhibitor
—Blocks negative regulators of Tcell function
—Inh PD-1 (nivolumab, pembrolizumab, cemiplimab, dostarlimab)
Or
—Inh PD-L1 (atezolizumab, avelumab, durvalumab)

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14
Q

Cyclophosphamide

A

(Cytoxan)
—Anti-neoplastic, Alk agent, Anti-rheumatologic
AE: N/V, Alopecia, Nephrotic, Myelosuppression
NB: Increase hydration and increase frequency of urination reduces risk of bladder toxicity and cystitis
—Consider antimicrobial ppx

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15
Q

Dasatinib

A

(Sprycel)
MOA: TKI
Oral
AE: N/V/D/F/P(bone)/F

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16
Q

Dacarbazine

A

MOA: Alk agent (MTIC), causes double strand breaks and apoptosis
AE: Myelosuppression (DLT), N/V (DLT)
Uses: Hodgkin Lymphoma
Nadir: 21-25 days

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17
Q

DARatumumab

A

(DARzalex)
MOA: Targets CD38 (often highly expressed on MM cells)
MP: special blood type testing prior because can make future testing inaccurate

NB: Darzalex faspro SQ has mandatory 4hr observation
2nd injection is 1 hour
MUST have type and cross prior
Also, will need IV access just in case.

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18
Q

Degarelix

A

(Firmagon)
MOA: GnRH antagonist (Gonadotropin Releasing Hormone)
Given SQ Q28d

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19
Q

Denosumab

A

(Xgeva, Prolia)
MOA: RANK LIGAND inh. Inh bone reabsorption. Used for prevention of skeletal mets and bone loss
NB: ORAL EXAM PRIOR TO TX, then monitored.

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20
Q

Docetaxel

A

(Taxotere)
MOA: Plant alk. Destabilizes microtubules
AE: Neuropathy, mucositis, fluid retention, myelosuppression (DLT)
NB: Premed with Dex
Nadir: 7 days

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21
Q

Doxorubicin Hcl

A

(Adriamycin)
MOA: Topoisomerase II inhibitor
AE: Myelosuppression, Mucositis, N/V, Cardiac, Transient LFTs,
MP: ECHO prior to tx, High risk with CHF. HBV screen.
NB: Red/orange/pink/brown urine
—Liposomal delivery less toxic but more frequent PPE, increased acute reactions
—Radiation Recall
Nadir: 10-14d

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22
Q

Durvalumab

A

(Imfinzi)
CPI
MOA: binds to PD-L1
NB: Steroids can reduce benefits of tx with this agent—But you treat toxicity with Steroids.

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23
Q

Enzalutamide

A

(Xtandi)
MOA: Androgen receptor signaling inhibitor. Leads to apoptosis.
NB: Unique, as there is no known agonist properties
Daily Oral.

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24
Q

Flurouracil

A

(5FU)
MOA: Pyrimidine analog
AE: >30% N(DLT)/V/D, decr appetite, mucositis(DLT), myelosuppression,alopecia
<30% PPE
Given IV, often sent home with pump for 2 days
Nadir 9-14d

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25
Q

Oxaliplatin

A

AE: COLD intolerance, neuropathy(DLT), myelosuppression, incr LFTs
Nadir: 10-14d

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26
Q

PPES

A

Palmoplantar Erythrodysesthesia

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27
Q

Ribociclib

A

(Kisqali)
MOA: Cyclin-dependent Kinase inh (esp. CDK4-&6).
–Given with aromatase inh synergistic effects on cancer
MP: EKG at baseline, 2 weeks and 4wks (prior to C2D1)
Uses: Br Cancer
Oral: 600mg 1 po QD x 21d, 28 d cycle.

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28
Q

R-EPOCH

A

Rituximab
Etoposide phosphate
Prednisone
Oncovin (vincristine sulfate)
Cyclophosphamide
Doxorubicin Hydrochloride
Used to treat certain types of non-Hodgkin lymphoma.

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29
Q

Rituximab

A

Rituxan
Uses: non-Hodgkin lymphoma, CLL, some rheumatoid
AE: CRS, TLS, AKI, PML (d/t reactivating JC virus), HBV reactivation,
MP: CBC w/ diff. Lytes.
NB: TLS.
MOA: 1.Binds to CD20 proteins on surface B cells. Doubles kill rate by NK cells.
2. Ab mediated toxicity
3. Compliment mediated toxicity

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30
Q

MPN

A

Myeloproliferative neoplasm

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31
Q

Imatinib

A

(Gleevec)

MOA: Inh BcrAbl TK (works on BcrAbl positive and Philadelphia positive cells)
Uses: CML
NB: Monitor for CHF!!!

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32
Q

Trastuzumab deruxtecan

A

(Enhertu)
MOA:is an antibody-drug conjugate consisting of the humanized monoclonal antibody trastuzumab (Herceptin) covalently linked to the topoisomerase I inhibitor deruxtecan (a derivative of exatecan).[11][12] It is licensed for the treatment of breast cancer or gastric or gastroesophageal adenocarcinoma. Trastuzumab binds to and blocks signaling through epidermal growth factor receptor 2 (HER2/neu) on cancers that rely on it for growth. Additionally, once bound to HER2 receptors, the antibody is internalized by the cell, carrying the bound deruxtecan along with it, where it interferes with the cell’s ability to make DNA structural changes and replicate its DNA during cell division, leading to DNA damage when the cell attempts to replicate itself, destroying the cell
MP: ILD/pneumonitis, CRS,

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33
Q

Epcoritamab-bysp

A

(Epkinly)
MOA: CD20 directed, CD3 T-cell engager
MP: CRS, ICANS
Route: SQ
Uses: DLBCL

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34
Q

TrasTUzumab

A

(Herceptin)
MOA: HER2 (inh cells which over express HER2)
MP: ECHO
AE: Card, Pn, CMP (DLT)

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35
Q

HER2

A

Human epidermal growth factor receptor 2.

Over-expression is also known to occur in
breast cancer, ovarian, stomach, adenocarcinoma of the lung, uterine, testicular germ cell, gastric, and esophageal tumours.

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36
Q

ICANS

A

Immune-effector cell-associated neurotoxicity syndrome
In general, it is thought that systemic inflammation and high levels of circulating cytokines result in endothelial cell activation and blood-brain barrier (BBB) disruption, which in turn causes an inflammatory cascade within the central nervous system (CNS), subsequent alterations in cortical and subcortical function, and diffuse cerebral edema in some cases.

Both ICANS and cytokine release syndrome (CRS) are considered an enhanced or supraphysiologic immune response to immune-modulating therapy that activates or engages T cells and/or other immune effector cells (IECs). CAR-T-related ICANS is commonly associated with, and follows, CRS, suggesting a potential mechanistic link. Clinical correlates of severe ICANS often overlap with severe CRS, including elevations in C-reactive protein (CRP), ferritin, and cytopenias.

While there was early speculation that neurotoxicity was antigen specific, since ICANS was observed both with the CD19-specific T cell engager, blinatumomab, and with CD19-specific chimeric antigen receptor T (CAR-T) therapies, subsequent reports have clearly identified ICANS in other, non-CD19-associated applications and diseases. Based on one clinical trial experience, it is possible that some delayed toxicities may be antigen specific, however.
Endothelial activation and disruption of the BBB have been identified as potential mechanisms. The angiopoietin (ANG) and angiopoietin receptor (TIE) axis is disrupted during an initial inflammatory insult, likely mediated, in part, by tumor necrosis factor alpha (TNF-alpha), interleukin (IL) 6, and IL-1. This results in endothelial activation and microvascular permeability, including BBB breakdown. With increased BBB permeability, patients with severe ICANS also exhibit elevated CNS levels of cytokines, protein, and T cell infiltrates

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37
Q

BiTEs

A

Bi-specific T-cell engagers

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38
Q

RARA

A

Retinoic acid receptor alpha.
(Part of cell cycle)
Translocations that always involve rearrangement of the RARA gene are a cardinal feature of acute promyelocytic leukemia. The most frequent translocation fuses the RARA gene with the PML gene

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39
Q

BCR-ABL and The Philadelphia chromosome (translocation).

A

Chrom 22, esp CML cells
This chromosome is defective and unusually short because of chrom 9&11 (BCR to ABL1, creates fusion gene called BCR-ABL1).
Hybrid protein = TK signaling stuck in on position. Uncontrolled cell division.

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40
Q

Olaparib

A

MOA: is a poly (ADP-ribose) polymerase (PARP) enzyme inhibitor, including PARP1, PARP2, and PARP3.
CBC at baseline and monthly
Monitor for signs/symptoms of venous thrombosis, pulmonary embolism, and pneumonitis
Monitor for signs of acute myeloid leukemia/myelodysplastic syndrome
HBV screening

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41
Q

Zometa

A

Asa ppx 81mg min

42
Q

Lenalidomide

A

(Revlimid)
MP: CBC, CMP, TSH,
TLS, Screening HBV,
Dosing: 10-25 mg PO daily,
MOA: 1.It selectively inhibits secretion of proinflammatory cytokines.
2.Enhances cell-mediated immunity by stimulating proliferation of anti-CD3 stimulated T cells.
3.Inhibits trophic signals to angiogenic factors in cells.
[The addition of lenalidomide to rituximab increases antibody dependent cell-mediated cytotoxicity in follicular lymphoma and marginal zone lymphoma and increases tumor cell apoptosis in follicular lymphoma (compared to rituximab alone)]
AEs: BM suppression (BBW), thromboembolic events (BBW), peripheral edema, peripheral neuropathy, Gl upset, rash
Dosing: 10-25 mg PO daily
NB: Clinical pearls: Must be registered w/ REMS program (RevAssist), consider anticoagulation px when used w/ dexamethasone after assessment of RFs

43
Q

Abraxane

A

Protein bound paclitaxel

— Pn monitoring

44
Q

Ipinivo

A

(Ipilimumab & Nivolumab)
MOA: CTLA-4 blocker & PD-1 inh
CPI

45
Q

Etoposide

A

MOA: Topoisomerase II inh
AE: myelosuppresson/ANC (DLT), infusion hypotn
Nadir 9-14days
NB: Risk of AML 2-3 yrs after tx

46
Q

Ipilimumab

A

(Yervoy)
MOA: CTLA-4 (down regulates T-cell activation).
Blocking CTLA-4 -> incr activation T cells & proliferation
CPI

47
Q

Irinotecan

A

MOA: Topoisomerase I inh
AE: D(DLT), myelosuppression, N/V/F, alopecia, LFTs, Tbili
NB: D <24 hrs = acute cholinergic effect 2/2 inh of acetylcholinesterase: tx w/ atropine
D >24hrs = d/t mucosal tox: tx with imodium and +/- octreotide

48
Q

Gemcitabine

A

(Gemzar)
MOA: Antimetab, gets taken into DNA (F-up DNA)
AE: myelosuppression (DLT), edema, sob, flu sx, LFTs

49
Q

Imatinib

A

(Gleevec)
MOA: ihh Bcr-Abl TK (works on Bcr-Abl+ and Philadelphia + cells)
MP: CBC, CMP, LDH, Screen HBV
Oral: w/ renal adjustments
NB: Monitor for CHF!!!

50
Q

Ruxolitinib

A

(Jakafi)
MOA:Ruxolitinib is a Janus Associated Kinases (JAKs), JAK1 and JAK2 inh.
Uses: Myelofibrosis, Polycythemia Vera.GVHD.
MP: CBC,CMP, HBV screen, PPD, screen HSV, monitor for VTE
NB:May lead to decreased expression of inflammatory cytokines in colon homogenates and decreased immune cell infiltration in the colon. Taper off.

51
Q

FOLFOX

A

Folinic acid (leucovorin)–enhances 5fu
Flurouracil
Oxaliplatin

52
Q

FOLFIRI

A

Folinic acid (leucovorin)–enhances 5fu
Flurouracil
Irinotecan

HOLD FOR ANC <1.5!!!

53
Q

FOLFIRINOX

A

Folinic acid (leucovorin)–enhances 5fu
Flurouracil
Irinotecan
Oxaliplatin

54
Q

Hydroxyurea

A

(Hydrea)
MOA: Antimetab– inh G1/S phase. Keeps in G1 and inh repair DNA
AE: myelosuppression
MP: Monitor liver and CMP

55
Q

Mirvetuximab

A

(Elahere)
MP: CBC, CMP, preg Ophth exam, every other cycle. Pneumonitis. Neuropathy. Screen HBV.
Uses: Fra positive Ovarian Ca
MOA: Mirvetuximab soravtansine, antibody-drug conjugate. 3 parts. Folate receptor mab, which consists of 3 components, a folate receptor alpha (FRα)-directed monoclonal antibody (IgG1 subtype), a small molecule anti-tubulin agent DM4 (a maytansine derivative), and a linker that covalently attaches DM4 to the mirvetuximab antibody.
Binding FRα, mirvetuximab soravtansine, taken in, intracellularly releases DM4, disrupts the microtubule network.

56
Q

PerTUzumab

A

(Perjeta)
MOA: Targets Human Epidermal GFr 2 (HER2).
MP: Echo
AE: Card tox, Diarrhea
NB: Binds @ diff HER2 site than herceptin(trastuzumab) = better inh

57
Q

Venetoclax

A

MP: CBC, CMP, PG test, TLS risk evaluation. HBV.
MOA: Cytotoxic to cells overexpress BCL-2 (anti-apoptotic protein), common in CLL and AML cells. BCL-2 assoc w/ chemo resistance.V directly binds to BCL-2 protein ->restores apoptosis.

58
Q

Mogamulizumab:

A

MP: PG test. Watch for derm tox. HBV.
MOA:
First in class. Binds to C-C chemokine receptor 4 (CCR4).
CCR4 mediates cell trafficking of lymphocytes to skin and various organs. M binding to CCR4 targets a cell for antibody-dependent cellular cytotoxicity (ADCC).

59
Q

(BiTEs).

A

Bi-specific T-cell engagers (BiTEs).
Bispecific monoclonal antibodies.
MOA:Links T cells directly to Tumor cells; by producing proteins like perforin and granzymes, independently of the presence of MHC I or co-stimulatory molecules. These proteins enter tumor cells and initiate the cell’s apoptosis

60
Q

Abemaciclib

A

Verzenio
MP:CBC, PG test, LFTs, diarrhea, pneumonitis, VTE, HBV
MOA:small molecule cyclin-dependent kinase (CDK) inhibitor which is selective for CDK 4 and 6.
Blocks retinoblastoma tumor suppressor protein phosphorylation and prevents progression through the cell cycle, resulting in arrest at the G1 phase.

61
Q

(Tebentafusp)

A

Kimmtrak
MP:HLA-A02:01 genotyping test. ALT, AST, total bili. PG test. HBV. CRS. First 3 infusions, monitor >16hrs after complete.
MOA: BiTE. Binds to a gp100 peptide presented by HLA-A02:01 on the surface of uveal melanoma tumor cells. Then recruits and activates polyclonal T-cells to release inflammatory cytokines and cytolytic proteins, resulting in direct lysis of uveal melanoma tumor cells.

62
Q

Asciminib

A

Asciminib
(Scemblix)

MP CBC q2wks x3mos, lipase and amylase monthly, Preg test. BP. CVD risk factors. HBV

MOA: Asciminib potently inh BCR-ABL1.

Uses: Philadelphia chromosome positive chronic CML (Ph+CML), previously txd w/ 2 or more TKIs

63
Q

Zanubrutinib

A

(Brukinsa)
MOA: Bruton tyrosine kinase (BTK) inh.
BTK is a signaling molecule of the B-cell antigen receptor and cytokine receptor pathways.
BTK signals activation of pathways necessary for B-cell proliferation, trafficking, chemotaxis, and adhesion.
Zanubrutinib inhibits malignant B-cell proliferation and reduces tumor growth.
MP: CBC, EKG, Cmp, HBV
ORAL
Uses: Lymphomas, CLL

64
Q

Alpelisib

A

Alpelisib
(Piqray)
MOA: PI3K inhibitor.
—inhibits cell lines harboring a PIK3CA mutation.
Combination of alpelisib with fulvestrant has synergistic antitumor activity in PIK3CA-mutated, estrogen receptor-positive models.
MP: Hyperglycemia.
FBG weekly, then monthly.
HbA1c, HBV, cbc, cmp, pneumonitis, colitis,
Uses: Br Ca
NB: PIK3CA related overgrowth spectrum (?)

65
Q

Chromogranin A

A

Chromogranin A, due to its primary expression throughout the neuroendocrine system, is a widely accepted biomarker for the assessment of neuro-endocrine tumors. It has been traditionally used in the management of patients with tumors of gastro-enteropancreatic origin.

66
Q

Ibrutinib

A

Ibrutinib
MOA: Bruton’s tyrosine kinase (BTK), an integral component of the B-cell receptor (BCR) and cytokine receptor pathways.
MP: Baseline ecg, Assess for risk of TLS, Pregnancy test, BP, CBC, CMP, Echo if high risk,
ORAL
NB: Avoid grapefruit, grapefruit juice, and Seville oranges during therapy.

67
Q

Pembrolizumab

A

Pembrolizumab
(Keytruda) ICI
MOA: binds to PD-1
AE: Immune mediated toxicities
(tx IMT w/ pred 1-2mg/kg/d)
— call, lighters, thyroid, hepatitis, pneumonitis, nephritis, mucositis,
MP: TSH, CBC, CMP,

68
Q

Acalabrutinib

A

(Calquence)

MOA: Bruton TKI. Binds @ BTK site.
Uses: CLL, SCLymphoma
MP: cbc, afib/aflutter
Oral: 100mg bid

NB: avoid PPIs/H2 blockers
Also – – raises risk of bleeding with surgery so hold 3d prior & 3d after

69
Q

ABVD

A

Doxorubicin (adriamycin) + Bleomycin + Vinblastine + Dacarbazine

—Q28d, IV ~3hrs total
AE: —Alopecia (15-60%. Starts 10-14d, gen grows back)
—decr WBCs (10-38%)
—n/v (9-15%)
—mucositis (1-16%)
—dry cough (11%)
—infection (2-11%)
—anemia (1-7%)
—SOB (3%)
—Pn (1-3%)
—decr platelets (0-2%)

  • Often given with the goal of cure*
70
Q

Afatinib

A

(Gilotrif)
MOA: TKI -> EGFR, HER2,HER4
MP: EGFR mutation status, HPV, UVEF, opth sx monitoring

71
Q

Arsenic + ATRA

A

Arsenic + ATRA
Arsenic Trioxide (ATO) is given at 0.15 mg/kg/day IV 5 days a week for 4 weeks on (i.e. total of 20 ATO infusions) and then 4 weeks off for a total of 4 of the 8 week courses.

Tretinoin (ATRA) is given at 45 mg/m2/day split into two doses per day. It is given Days
1-14 and then held Days 15-28 then restarted Day 29-42 and held Days 43-56.

This corresponds to the 4 weeks of ATO infusions followed by 4 weeks off (i.e. 8 week cycles). Repeat for a total of 4 of these dosing schedules. The next Days 1-14 etc cycle of ATRA begins with the start of the next 4 week set of Arsenic infusions. The ATRA is NOT GIVEN ON DAYS 29-42 OF THE LAST CYCLE OF ARSENIC INFUSIONS (i.e not given during the 4 weeks off after the 4” set of Arsenic infusions)

Pre-arsenic medications
—Prochlorperazine 5-10mg oral x 1 prior to arsenic- (may be omitted if patient is without any nausea)
—Lorazepam 0.5 mg-1mg oral as needed for N/V
—Zofran 4-8 mg po/IV as needed for nausea unrelieved by above measures

IV arsenic
0.15mg/kg/dose arsenic trioxide (ATO) IV daily Mon-Fri
***mg IV over 1-2 hours,
for 4 weeks on
then 4 weeks off
for a total of 4 of the 8 week cycles. Schedule is 5 days per week infusions for a total of 20 doses each cycle.

Prophylaxis (for ANC<1,000)
Acyclovir 800 mg PO daily Levaquin 500 mg PO daily
Micafungin 100mg IV daily Mon-Fri

Complete Metabolic Panel and Magnesium level at least 3x/week. May do 2x/week during weeks of ATRA or no therapy IF STABLE
Goal is to keep Mg>2.0 and K>4.0
—If serum Mg < 1.6 then 4gm IV Magnesium x1
—If serum Mg<1.8 then 2gm IV magnesium x1
—If serum K<3.5 then 40 mEq IV KCI and PO 40 mEq KCI
—If serum K<3.7 then 40 mEq PO KCI

Transfusion
CBC with differential at least 3x/week, APTT, PT, Fibrinogen levels (Coag Panel) every Monday.
CBC with Diff may be done twice a week during weeks of ATRA or no therapy. Continue weekly coags.
For Hct<24 tranfuse 1 unit irradiated/leukoreduced PRBCs
For plt<30 transfuse 1 irradiated/leukoreduced platelet pheresis product
For fibrinogen <150 transfuse 1 unit cryoprecipitate
Monitoring

EKG Monday and Thursday during the weeks of Arsenic therapy to monitor QTc. QTc interval
>460msec for women is considered prolonged.
—If prolonged QTc:
First discontinue other medications known to prolong the QTc
Replete Mg>2.0 K>4.0
—If QTc remains prolonged then discontinue ATOOnce QTc normalized then resume ATO at 0.075 mg/Kg (50%) for 7 days
—If no further prolongation then resume ATO at 0.11 mg/kg (75%) for a second week.Thereafter, if no prolongation occurred, resume ATO at full dose.

LFTs 3x/week to monitor for hepatotoxicity. (Will be included in CMP). Grade 3-4 hepatotoxicity defined as an increase in serum bili and/or SGOT and/or alk phos >5 times the normal upper limit.
If increase then: temporary discontinuation of ATRA and ATO —once decreased below 4 times the normal upper level, then resume ATRA
—if stable x2 days then resume ATO at 50% (0.075 mg/kd/d) for 7d
—if continued stability then resume ATO at 0.11 mg/kg (75%)for 2nd wk 
—Thereafter, resume ATO full dose
—If reappearance of hepatotox, discontinue medications

Complete Metabolic Panel and Magnesium level at least 3x/week. May do 2x/week during weeks of ATRA or no therapy IF STABLE
Goal is to keep Mg>2.0 and K>4.0
- If serum Mg < 1.6 then 4gm IV Magnesium x1
If serum Mg<1.8 then 2gm IV magnesium x1
If serum K<3.5 then 40 mEq IV KCI and PO 40 mEq KCI
If serum K<3.7 then 40 mEq PO KCI
Transfusion
CBC with differential at least 3x/week, APTT, PT, Fibrinogen levels (Coag Panel) every Monday.
CBC with Diff may be done twice a week during weeks of ATRA or no therapy. Continue weekly coags.
For Hct<24 tranfuse 1 unit irradiated/leukoreduced PRBCs
For plt<30 transfuse 1 irradiated/leukoreduced platelet pheresis product
For fibrinogen <150 transfuse 1 unit cryoprecipitate
Monitoring
EKG Monday and Thursday during the weeks of Arsenic therapy to monitor QTc. QTc interval
>460 msec for women is considered prolonged.
If prolonged QTc:
First discontinue other medications known to prolong the QTc
Replete Mg>2.0 K>4.0
- If QTc remains prolonged then discontinue ATO
- Once QTc normalized then resume ATO at 0.075 mg/Kg (50%) for 7 days
If no further prolongation then resume ATO at 0.11 mg/kg (75%) for a second week.
- Thereafter, if no prolongation occurred, resume ATO at full dose.
LFTs 3x/week to monitor for hepatotoxicity. (Will be included in CMP). Grade 3-4 hepatotoxicity defined as an increase in serum bilirubin and/or SGOT and/or alkaline phosphatase >5 times the normal upper limit.
If increase then:
- temporary discontinuation of ATRA and ATO
once decreased below 4 times the normal upper level, then resume ATRA if stable x2 days then resume ATO at 50% (0.075 mg/kd/d) for 7 days if continued stability then resume ATO at 0.11 mg/kg (75%) for a second week.
Thereafter, resume ATO at full dose
- If reappearance of hepatotoxicity, discontinue medications

72
Q

Avatrombopag

A

(Doptelet)
MOA: TPO receptor agonist, incr megakaryocytes
Uses: ITP

73
Q

Avelumab

A

(Bavencio)
MOA: PD-L1 (CPI)
Uses: Renal cell, urothelial carcinoma, merkel cell
AE: —fatigue (21%)
—infusion reaction (21)
—weakness (11)
— Nausea (11)
— Diarrhea (9)
— rash (9)
— decr thyroid (7)
— itch (7)
—decr appetite (5)
— liver (2-5)
— lung (2)
— arthritis (2)
—eye irritis (2)

74
Q

Axitinib

A

(Inlyta)
MOA: 2nd gen TKI -> VEGFR-1,2,3 inh AngioNeoGen
Oral
MP:LFTs,tsh, UA protein, chf
AE: incr SCr, Htn, incr LFTs, impaired healing
NB: similar to avastin

75
Q

Bendamustine

A

MOA: Alk agent (nitrogen MUSTard). Decr dna
Uses: lymphoma, MM
MP: CBC, CMP, LFT, uric acid, potassium, pregnancy test, PML*, HPV, TLS, Bili
AE: Myelosuppression
Nadir: 21days

NB: Allopurinol

  • progressive, multifocal, encephalopathy, (JC virus)
76
Q

Bleomycin

A

MOA: inh synthesis DNA -> dbl and single strand breaks
MP: PFTs,

77
Q

Cabazitaxel

A

(Jevtana)
MOA: microtubule inh, arrests cell division
MP: cbc, cmp Qwk first cycle, then each tx
AE: —anemia (97%)
—neutropenia (94)
—decr plat (47)
—diarrhea (47)
—fatigue (37)
—nausea (34)
—vomiting (23)
—constipation (20)
—hematuria (17)
—Pn (14)
—abd pain/fever/sob (12)
—alopecia (10)
—discontinued (18)

78
Q

Fotivda

A

(Tivozanib)
MOA: TKI

79
Q

Cladribine

A

(Leustatin)

NB: Do not take with etoh

80
Q

Cytarabine

A

NB: TLS risk.

81
Q

Teclistamab

A

TECVAYLITM
(Teclistamab) is the first T-cell redirecting bispecific antibody approved for patients with MM. Targeting both CD3 receptor complex on T cells and BCMA on myeloma cells, teclistamab leads to T-cell activation and subsequent lysis of BCMA+ cells.
AE:
—ICANS
—CRS

For CRS, Tocilizumab

82
Q

Lanreotide

A

A somatostatin used to suppress neuroendocrine tumors

83
Q

Vincristine

A

Oncovin
(chOp)
MOA: anti-microtubular agent, vinca alkaloid parentheses periwinkle and parentheses
AE: N/V, neuropathy, alopecia

84
Q

Irinotecan

A

Irinotecan
MOA: topoisomerase inh.
AE: diarrhea (dlt), milo, suppression, and/V, fatigue, alopecia, increase LFTs/bili

NB: D>24hrs= acute colonic effect 2/2 inh acetylcolonesterase: tx w/ atropine
D>24hrs D/T Yocal talks; tx W/Imodium +/- octreotide

85
Q

Ramucirumab

A

(Cyramza)
MOA: VEGFR2

MP: LFTs, UA protein, TSH, CBC, pregnancy test, BP, baseline echo, HBV

86
Q

Cabozantinib

A

(Cabometyx)
MOA: TK, inhibits pro invasive receptor, TK, VEGF
AE: neuropathy.
Oral

NB; No grapefruit.

87
Q

Isatuximab

A

(Sarclisa)
MOA: mab, AntiCD38
Premed:
-Dex
- Acetaminophen 650 mg to 1 g
- An H2 antagonist.
- Diphenhydramine 25 to 50 mg IV or oral (or equivalent); for at least the first 4 infusions, the IV route is preferred.

88
Q

Nivolumab

A

(Opdivo)
MOA: ICI, PD-1
Uses: GI, Hepatic, Hodgkin lymphoma, melanoma, head/neck, mesothelioma, RCC, NSCLC, urothelial

89
Q

Momelotinib

A

(Ojjaara)
MOA: TKI, Janus kinase inh, Activin A type 1 receptor inh.
(JAK1/JAK2, ACVR1)
Indications: Myelofibrosis
AE: <10%

90
Q

Lurbinectedin

A

(Zepzelca)
MOA: Alk agent
AE: decr Mg, Na, glucose, pancytopenia, LFTs, Fatigue, myalgia, Creatinine, cough,

91
Q

Enfortumab vedotin

A

(Padcev)
MOA: Antibody-drug conjugate.
Enfortumab mab locks onto nectin-4 (express on urothelial cells), released payload MMAE (which is too toxic by itself— must be delivered directly to the cancer cells).
NB: MMAE 200x more toxic than vinblastine.

92
Q

MMAE

A

MMAE (monomethyl auristatin E) which is too toxic by itself— must be delivered directly to the cancer cells).
NB: MMAE 200x more toxic than vinblastine.
Antimototic
NB: vedotin refers to MMAE and the linking structure to Ab.

93
Q

Tucatinib

A

(Tukysa)
Used for HER2-positive breast cancer.
MOA: small molecule inhibitor of HER2.
Usually given with trastuzumab and capecitabine.

94
Q

Amivantamab

A

(Rybrevant)
MOA: bispecific monoclonal antibody used to treat NSCLC
EGFr, and mesenchymal–epithelial transition receptor METr, directed antibody.

95
Q

Palbociclib

A

(Ibrance)
MOA: reversible? CDK inh selective for CDK 4&6..
AE: neutropenia 75%! Nausea and diarrhea, alopecia, stomatitis.
Oral: daily. typically 21D on, 70 off.

96
Q

Viոorеlbiոе

A

MOA: semisynthetic vinca alkaloid.

97
Q

Cetuximab

A

Erbitux
MOA: EGFR inh.
Use: H&N SCC, colorectal cancer

98
Q

Panitumumab

A

(vectibix)
MOA: targets EGFR.

Uses: colorectal ca.

dermatologic or soft tissue toxicity:
Grade 3 toxicity (first occurrence): Withhold 1 to 2 doses; if reaction improves to <grade 3, resume therapy at initial dose.
Grade 3 toxicity (second occurrence): Withhold 1 to 2 doses; if reaction improves to <grade 3, resume therapy at 80% of initial dose.
Grade 3 toxicity (third occurrence): Withhold 1 to 2 doses; if reaction improves to <grade 3, resume therapy at 60% of initial dose.
Grade 3 toxicity (fourth occurrence), grade 3 toxicity that does not recover to <grade 3 after withholding 1 or 2 doses, or grade 4 toxicity: Permanently discontinue.
Ocular toxicity (acute or worsening keratitis, ulcerative keratitis, or corneal perforation): Interrupt or discontinue treatment.
Pulmonary toxicity:
Acute onset or worsening pulmonary symptoms: Interrupt treatment.
Interstitial lung disease: Permanently discontinue treatment.
Dosing: Older Adult
Refer to adult dosing.
Adverse Reactions
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Reported adverse reactions are for adults.
>10%:
Dermatologic: Acne vulgaris (14%), acneiform eruption (57%), erythema of skin (66%), exfoliative dermatitis (18%), paronychia (25%), pruritus (58%), skin fissure (20%), skin rash (22%), skin toxicity (90%; severe dermatological reaction: 15%)
Gastrointestinal: Nausea (23%; grade 3/4: <1%), diarrhea (21%; grades 3/4: 2%), vomiting (19%; grade 3/4: 3%)
Nervous system: Fatigue (26%)
Ophthalmic: Ocular toxicity (16%)
Respiratory: Cough (15%), dyspnea (18%)
Miscellaneous: Fever (17%)

99
Q

Sotorasib

A

(LumaKRAS)
MOA:
Uses: kras G12C mutated NSCLC, after progression on firstline tx

100
Q

Osimertinib

A

(Tagrisso)
MOA: EGFR TKI.
MP: baseline QTc
NB: opth tox, card tox, GI tox, pulm tox.

101
Q

Lorlatinib

A

(Lorbrena)

MOA: TKI.
Uses: NSCLC

AE: edema, PN, weight gain, cognitive effects, fatigue, dyspnea, arthralgia, diarrhea, mood effects, hypercholesterolemia, hypertriglyceridemia, and cough.

102
Q

Vinblastine

A

Vinblastine
AE: myelosuppression (DLT), nadir5 to 10 days, constipation, alopecia, HTN

Oncology (1 decks)

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