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Heme/Lymph Exam > Chemo 2 > Flashcards

Chemo 2 Flashcards

1
Q

topoisomerase I inhibitors - examples

A

*camptothecins:
-irinotecan
-topotecan

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2
Q

topoisomerase II inhibitors - examples

A
  1. anthracyclines:
    -daunorubicin
    -doxorubicin
    -idarubicin
    -epirubicin
  2. epipodophyllotoxins
    -etoposide
  3. other: mitoxantrone
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3
Q

topoisomerase I inhibitors (camptothecans): MOA

A

*disrupt DNA strands by binding to the DNA-topoisomerase I complex and preventing the resealing of DNA (allows the cut in the DNA but does not allow it to be repaired)

recall: topoisomerase I relaxes supercoiled DNA by creating a single nick in the DNA and repairing it

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4
Q

topoisomerase II inhibitors (anthracyclines, epipodophyllotoxins, mitoxantrone): MOA

A

*disrupt DNA strands by binding to the DNA-topoisomerase II complex and preventing the resealing of DNA (allows the cuts in the DNA but does not allow them to be repaired)

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5
Q

camptothecins - toxicities

A

*severe diarrhea:
-irinotecan > topotecan

*myelosuppression

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6
Q

anthracyclines - MOA

A

*topoisomerase II inhibitors (cuts both strands of one DNA double helix)

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7
Q

examples of anthracyclines

A

*daunorubicin
*doxorubicin
*idarubicin
*epirubicin

recall: anthracyclines are topo II inhibitors

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8
Q

anthracycline toxicities

A

*myelosuppression
*cardiotoxicity (dilated cardiomyopathy)
*extravasation injury:
-vesicant
-treat with dexrazoxane and cold compress
N/V
**red/orange urine discoloration

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9
Q

cardiotoxicity with anthracyclines (“-rubicins”)

A

*MOA: accumulation of oxygen-derived free radicals in the cardiac tissue, causing lipid, protein, and DNA damage
*acute: decreased contractility, pericarditis, myocarditis, arrythmia, elevation of biomarkers
*early-onset chronic progressive: tachycardia, ventricular dilation, exercise intolerance, pulmonary and venous congestion
*late-onset chronic progressive: ventricular dysfunction, conduction disturbances, arrythmias, CHF

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10
Q

prevention of cardiotoxicity associated with anthracyclines

A

*dexrazoxane: inhibit the iron-dependent free radical formation that can cause myocardial damage

*liposomal formulation:
-liposomal delivery system not as readily taken up by cardiac tissue, leading to decreased risk of cardiotoxicity

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11
Q

what drug is used IV to prevent cardiotoxicity associated with anthracyclines

A

dexrazoxane

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12
Q

mitoxantrone - overview

A

*similar mechanism to anthracyclines (topo II inhibitor)
*does NOT form free radicals: decreased risk of cardiotoxicity and extravasation
*blue-green urine discoloration

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13
Q

epipodophyllotoxins - overview

A

*example = etoposide
*MOA: inhibits topo II
*toxicities: myelosuppression, mucositis, hypotension

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14
Q

mitotic inhibitors - examples

A
  1. vinca alkaloids:
    -vincristine
    -vinblastine
    -vinorelbine
  2. taxanes
    -paclitaxel
    -docetaxel
    -cabazitaxel
  3. halichondrin B analog
    -eribulin
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15
Q

vinca alkaloids - MOA

A

*prevent the assembly of tubulin dimers into microtubules → prevent mitotic spindle formation
*cells accumulate in mitosis and undergo apoptosis

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16
Q

vinca alkaloids - toxicities

A

*vinBLASTine (and vinorelbine) = blast the marrow = MYELOSUPPRESSION

*vinCRIStine = crisps the nerves = NEUROTOXICITY or peripheral neuropathy

note - FATAL if given intrathecally (into the CNS)

17
Q

taxanes - MOA

A

*promote microtubule assembly
*interfere with microtubule disassembly
*stabilize microtubles → prevent mitotic spindle breakdown

18
Q

taxanes - toxicities

A

*myelopsuppression
*mucositis
*peripheral neuropathy
*hypersensitivity reactions

19
Q

eribulin - overview

A

*inhibits formation of mitotic spindles
*one of the mitotic inhibitors
*ADEs: neutropenia, alopecia, fatigue, peripheral neuropathy

20
Q

proteasome inhibitors - examples

A

*bortezomib
*carilzomib

21
Q

bortezomib - overview

A

*class: proteasome inhibitor
*MOA: REVERSIBLE binding of the proteasome → apoptosis
*toxicities: peripheral neuropathy, thrombocytopenia, neutropenia
note - subQ administration preferred due to less neurotoxicity

22
Q

carfilzomib - overview

A

*class: proteasome inhibitor
*MOA: IRREVERSIBLE binding of the proteasome → apoptosis
*toxicities: cardiac arrest/CHF; pulmonary HTN/dyspnea, thrombocytopenia

23
Q

traditional chemotherapy - drug classes

A

*platinums
*alkylating agents
*anthracycline
*topoisomerase inhibitors
*antitumor antibiotics

24
Q

targeted chemotherapy - drug classes

A

*monoclonal antibodies
*small molecule inhibitors

25
Q

rituximab - MOA

A

*chimeric antibody targeting CD20, most notably on B lymphocytes

26
Q

rituximab - toxicity profile

A

*infusion reactions
*tumor lysis syndrome
*lymphopenia
*infection

27
Q

EGFR/HER inhibitors

A

*monoclonal antibody:
1. trastuzamab - blocks HER2
-toxicities: reversible cardiotoxicity
2. cetuximab & panitumumab - HER1/EGFR
-toxicities: skin rash

*small molecule (tyrosine kinase inhibitor): erlotinib & gefitinib - targets HER1/EGFR tyrosine kinase
-toxicities: skin rash, diarrhea

28
Q

EGFR/HER inhibitors - toxicity trends

A

*if target is EGFR1 (HER1): skin toxicities (rash)

*if target is HER2 (EGFR2): cardiac toxicities

29
Q

BRAF inhibitors - MOA

A

disrupt downstream signaling that initiates from or proceeds to the BRAF domain

30
Q

BRAF inhibitors - examples

A

-vemurafenib
-dabrafenib
-encorafenib

31
Q

BRAF inhibitors - toxicities

A

*new primary malignancies
*BRAF (-) cancer
*uveitis/iritis
*rash, fatigue, nausea, diarrhea

32
Q

VEGF inhibitors - MOA

A

*inhibit blood vessel formation

33
Q

VEGF inhibitors - examples

A

*bevacizumab

34
Q

VEGF inhibitors - toxicities

A

*thromboembolic bleeding events and HTN

35
Q

tyrosine kinase inhibitors that target BCR-ABL - examples

A

*imatinib
*dasatinib
*nilotinib

36
Q

tyrosine kinase inhibitors that target BCR-ABL - toxicities

A

*drug interactions
*GI toxicities
*myelosuppression
*elevated LFTs
*edema
*myalgias

Heme/Lymph Exam (38 decks)

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