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Heme/onc > oncology drugs > Flashcards

oncology drugs Flashcards

1
Q

MOA of alkylating agents

A

Alkylation = covalent attachment of alkyl groups to other molecules

Major target of alkylation is N7 of guanine

Single base alkylation or cross-linking of DNA can occur

Leads to mismatched base pairs, prevention of DNA separation

No cell cycle specificity

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2
Q

alkylating agent toxicities

A

Myelosuppression (Febrile neutropenia)

Mucositis

Nausea/vomiting

Allopecia

Secondary malignancies

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3
Q

Mechlorethaminea

A

*historical drug–alkylating agent derivative of mustard gas

Toxicities include myelosuppression, alopecia, and nausea/vomiting (N/V)

Mechlorethamine cured many patients, but caused DNA damage, sterility in most patients, and increased the risk of secondary malignancies

Potent vesicant

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4
Q

cyclophosphamide

A

alkylating agent derivative of mustard gas

Prodrug. Activated by liver to active and toxic metabolites

IV and PO

Hemorrhagic cystitis: production of acrolein causes irritation to bladder wall. (Adequate hydration, Mesna with high doses)

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5
Q

ifosfamide

A

alkylating agent derivative of mustard gas. Analog of cyclophosphamide. Also requires hepatic activation to same active metabolites

Less potent, requires 4 x dose for efficacy

Increased production of acrolein accumulates in bladder and causes hemorrhagic cystitis

Administer with Mesna (IV/PO), hydration important.

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6
Q

Melphalan

A

alkylating agent derivative of mustard gas

Oral and IV

High dose (200 mg/m2) used for autologous HSCT

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7
Q

Bendamustine

A

Combination alkylating agent and purine analog

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8
Q

nitrosureas

A

alkylating agents

Lipophilic, good CNS penetration

Delayed myelosuppression, 4 week nadir

Severe N/V, pulmonary toxicity, hepatotoxicity

Carmustine implant: Gliadel Wafer

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9
Q

Dacarbazine

A

alkylating agent w/ good CNS penetration

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10
Q

Temozolamide

A

oral, converted to dacarbazine–>alkylating agent w/ good CNS penetration

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11
Q

platinum analogues

A

-alkylating agents (carboplatin, cisplatin, oxaliplatin)

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12
Q

cisplatin

A

alkylating agent, platinum analog

nephrotoxiticy, ototoxicity, N/V (Hydration, antiemetics)

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13
Q

Carboplatin

A

alkylating agent, platinum analog

Carboplatin: myelosupression, less N/V, neuropathy, nephrotoxocity than cisplatin

dosing based on renal function

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14
Q

Oxaliplatin

A

alkylating agent, platinum analog

acute: cold induced neuropathy, cumulative peripheral neuropathy

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15
Q

topoisomerase II inhibitors

A

Anthracyclines: daunorubicin, doxorubicin, epirubicin, idarubicin

mitoxantrone

etoposide

  • High affinity binding to DNA
  • Intercalates between base pairs, inhibits the activity of enzymes involved in DNA replication (topoisomerase II)
  • Anthracyclines form free radical compounds that damage biological macromolecules
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16
Q

topoisomerase I inhibitors

A

Camptothecins: irinotecan, topotecan

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17
Q

topoisomerase inhibitors MOA

A

Topoisomerases (I and II) are nuclear enzymes that unravel DNA for repair and replication

Specifically they participate in DNA replication and repair by:

  • cleaving and resealing the phosphodiester bonds that comprise the backbone of DNA (Topo II)
  • unwinding DNA (Topo I)

Inhibiting topoisomerases can induce DNA damage such as unrepairable strand breaks leading to cell apoptosis

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18
Q

anthracyclines: drugs?

toxicities?

A

doxorubicin, daunorubicin, idarubicin, epirubicin

CHF after a cumulative dose is reached, high/delayed emetogenicity, vesicants

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19
Q

topotecan

A

topoisomerase I inhibitor (undwinding DNA)

dose limited marrow suppression

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20
Q

irinotecan

A

topoisomerase I inhibitor

Diarrhea is a dose limiting side effect

  • Early form–Cholinergic syndrome treated with IV atropine
  • Late form–Direct GI toxicity. Loperamide 4 mg x 1, 2 mg q2hr. May cause serious dehydration
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21
Q

Bleomycin

MOA and toxicities

A

Bleomycin produces single and double strand breaks in DNA through the production of highly reactive free radicals

Toxicity: pulmonary fibrosis (avoid cumulative dose >400 units, current radiation/oxygen). Hyperpigmentation, rash, fever, allergic rxn.

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22
Q

antimicrotubule drugs

A

Vinca Alkaloids: vinblastine, vincristine, vinorelbine

Taxanes: docetaxel, paclitaxel

Epothilones: ixabepilone

Disrupt cell division in M phase

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23
Q

vinblastine, vincristine, vinorelbine

drugs

MOA

toxicities

A

vinca alkaloids

inhibit the formation of tubulin, which prevents polymerization into microtubules

inhibit cell division dring M phase cell cycle

Vincristine:
neurotoxicity, constipation
Max dose 2 mg/week

Vinblastine/vinorelbine:
Myelosuppression
Less neurotoxicity

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24
Q

docetaxel, paclitaxel, carbazitaxel

MOA

A

Taxanes bind to beta tubulin and stabilize the alpha and Beta tubulin heterodimers, preventing the breakdown of microtubules

disrupts cell division in M phase

Toxicities:

Require premedication with steroids due to solubilizing agents

Paclitaxel
Neuropathy
Albumin-bound paclitaxel (Abraxane), no solubilizer

Docetaxel
Fluid retention syndrome: dex 8 mg PO BID x 3 days

Cabazitaxel
Crosses BBB, not affected by P-glycoprotein

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25
Q

ixabepilone

A

epithalones bind to beta tubulin and stabilize the alpha and Beta tubulin heterodimers, preventing the breakdown of microtubules

disrupts cell division in M phase

Distinct tubulin binding site, not effected by Pgp

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26
Q

general MOA of antimetabolites

categories/drugs

A

Structurally these agents mimic their naturally occurring nucleotide cousins

S-phase specific

They work by one or a combination of the following:

  • inhibiting enzymes involved in nucleotide synthesis
  • inhibiting enzymes involved in DNA replication
  • replacing naturally occurring nucleotides in DNA that is actively being replicated. This serves to disrupt the -natural structure of DNA, causing apoptosis.

Folate Antagonists: methotrexate, pemetrexed, pralatrexate

Purine Analogues: cladribine, fludarabine, mercaptopurine, nelarabine, pentostatin, thioguanine

Pyrimidine Analogues: capecitabine, cytarabine, fluorouracil, floxuridine, gemcitabine

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27
Q

Methotrexate

A

folate antagonist

  • Inhibits dihydrofolate reductase (decreases reduced folates, inhibits thymidylate synthase)
  • IV, IM, IT, PO
  • Cleared renally, accumulates in third-space fluids
  • High-dose therapy: hydrate with bicarb containing fluids until urine pH > 7, leucovorin rescue, and monitor MTX blood levels, < .05 µM (5 x 10-8 M)
  • Mucositis, pneumonitis, renal failure, inc LFT’s
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28
Q

Thioguanine (6-TG) and mercaptopurine (6-MP)

A

purine analog

Oral agents

Liver toxicity, mucositis

Mercaptopurine metabolized by xanthine oxidase

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29
Q

Fludarabine, cladrabine, pentostatin

A

pyrimidine analogs

Immunosuppression (lymphopenia)

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30
Q

nelabarine

A

purine analog

neurotoxicity is dose limiting

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31
Q

cytarabine (Ara-C)

A

cytidine analog

flu-like syndrome, rash

High dose: HiDAC

  • marrow suppression
  • cerebellar toxicity
  • conjunctivitis (steroid eye drops)
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32
Q

Flourouracil (5-FU)

A

converted to F-FdUMP, inhibits thymidilate synthase (dUMP–>dTMP)

toxicity is dose and frequency dependent

  • intermittent bolus: myelosuppression
  • continuous: hand-foot syndrome

administration of leucovorin potentiates effects

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33
Q

capecitabine

A

oral agent converted to flourouracil

selectively activated by tumor cells

Toxiciites: hand-foot syndrome, GI

34
Q

5-azacitidine, decitabine

A

inhibits DNA methyltransferase

hypomethylates DNA

activates previously “silenced” tumor suppressor genes

  • inhibits angiogenesis, metastasis
  • allows apoptosis
    *
35
Q

general MOA of monoclonal antibodies

A

Disrupt signal transduction

  • neutralizing the ligand (bevacizumab)
  • inhibiting extracellular receptors (cetuximab, panitumab)

Direct Cytotoxicity (rituximab, alemtuzumab)

  • complement dependent
  • antibody dependent
  • induction apoptosis

Delivery of cytotoxic agents

  • radioactive moieties (tositumab, ibritumomab)
  • anti-neoplastic (brentuximab, vedotin)
36
Q

rituximab/ofatumumab

A

cytotoxic anti-CD20 antibody

CD20 on B lymphocytes

Present on >90% of all B cell NHL and leukemias

mediates ADCC and CDCC

ADE:

  • infusion reactions (titrate infusions)
  • tumor lysis syndrome

Ofatumumab binds to a different epitope on CD20

37
Q

Alemtuzumab

A

cytotoxic anti-CD52 antibody

CD52 on normal and malignant T cells, NK cells, monocytes, and macrophages

Used in refractory CLL, T-cell leukemia

ADE:

  • Infusion reactions, anaphylaxis
  • profound prolonged immunosuppression, HSV and PCP prophylaxis
38
Q

Ibritumomab and Tositumomab

A

anti-CD20 antibody conjugated to radioactive compounds

Use in Relapsed and/or refractory CD20-positive, follicular NHL

Avoid in patients with > 25% involvement of the bone marrow by lymphoma and/or impaired bone marrow reserve.

ADE: myelosuppresion, leukopenia (prolonged)

39
Q

brentuximab vedotin

A

Anti-CD30 antibody attached to monomethyl auristatin E (MMAE)

MMAE is a mitotic spindle poison

Used in Hodgkin, anaplastic large cell lymphoma

ADE: Infusion reactions, myelosuppression, peripheral neuropathy

40
Q

denileukin diftitox

A

anti-CD25 antibody (IL2-receptor) attached to diptheria toxin

used in persistent or recurrent cutaneous T-cell lymphoma

ADE: infusion reactions, vascular leak, flu-like syndromes, hepatotoxicity

41
Q

Trastuzumab/pertuzumab

A

anti-HER2/neu receptor antibody (signal blocking antibody)

HER2 overexpressed on 25% breast cancers

binding results in apoptosis and ADCC

ADE: infusion reactions, anaphylaxis

Trastazumab: cardiotoxicity, esp when used w/ cyclyophosphamide or anthracycline

42
Q

cetuximab/panitumab

A

Anti-EGFR antibody (signal blocking antibody)

EGFR overexpressed in many solid tumors

antibody binding results in inhibition of proliferation, growth, metastasis, and angiogenesis

enhances response to chemo and radiation

ADE: infusion reactions, anaphylaxis

  • skin toxicity may be severe
  • electroylyte imbalances
43
Q

bevacizumab

A

anti-VEGF antibody (signal blocking)

inhibits formation of new blood vessels in primary and metastatic tumors

ADE: infusion reactions, anaphylaxis

  • GI perforations tracheoesophageal fistulasand
  • circulatory: bleeding, arterial thrombosis, hypertension, impaired wound healing, proteinuria
44
Q

Ipilimumab

A

binds cytotoxicy T-lymphocyte-associated-antigen 4 (CTLA-4)

blockage of CTLA-4 augments T cell activation and proliferation

can result in severe and fatal immune-mediated adverse reactions due to T cell activation

ADE: colitis, hepatitis, toxic epidermal necrolysis

45
Q

tyrosine kinase inhibitors general

A

These enzymes are involved in cellular signaling pathways and regulate key cell functions such as proliferation, differentiation, anti-apoptotic signaling

Inhibitors occupy ATP binding site and prevent phosphorlyation of substrates

All are CYP3A4 substrates

46
Q

erlotinib

gefitinib

A

RTK inhibitor

inhibited EGFR (TK)

NSCLC

ADE: diarrhea, skin rash (correlates with efficacy)

47
Q

imatinib

A

intracellular TKI

inhibits BCR-ABL TK (philadelphia chr t(9;22))

used in CML

ADE: myelosuppression

48
Q

Dasatinib

A

Intracellular TKI

Inhibits BCR-ABL TK created by Ph chromosome translocation (9;22), PDGF, cKIT

Used in CML

Dasatinib also inhibits SRC kinase

toxicity is myelosuppression

49
Q

Nilotinib

A

Intracellular TKI

Inhibits BCR-ABL TK created by Ph chromosome translocation (9;22), PDGF, cKIT

Used in CML

Nilotinib more potent than imatinib

Toxicity: myelosuppression

50
Q

sunitinib

A

inhibits PDGFR and VEGFR

used in renal cell cancer

Toxicities: GI, skin discoloration, fatigue, hypertension, bleeding, CHF

51
Q

sorafinib

A

inhibits PDGFR and VEGFR

used in RCC and hepatocellular cancer

Toxicites: GI, rash, hypertension, bleeding, hand-foot syndrome

52
Q

lapatinib

A

Inhibits EGFR ad Her-2

Used in Her2+ breast cancer

Toxicities: diarrhea, decreased LVEF, QT prolongation (cardio)

53
Q

vemurafenib

A

BRAF inhibitor

melanoma w/ BRAF V600E mutation

54
Q

crizotinib

A

ALK inhibitor

ALK postiive NSCLC

55
Q

ruxolitinib

A

JAK inhibitor

used in myelofibrosis

56
Q

Vismodegib

A

hedgehog inhibitor

used in basal cell skin cancer

embryotoxic and teratogenic

57
Q

rapamycin

A

mTOR inhibitor

Binds to FK Binding Protein

FKBP-drug complex inhibits mTOR kinase activity

Decreased production of Hypoxia Inducible Factor, VEGF, PDGF, TGF

58
Q

Temsirolimus

A

mTOR inhibitor

Binds to FK Binding Protein

FKBP-drug complex inhibits mTOR kinase activity

Decreased production of Hypoxia Inducible Factor, VEGF, PDGF, TGF

Toxicities:

  • hyperglycemia
  • inc. TG/cholesterol
  • rash, asthenia, mucositis
    *
59
Q

all-trans-retinoic acid (ATRA)

A

ATRA provides high levels of retinoic acid

Induces differentiation and maturation of acute promyelocytic cells to normal myelocyte cells

used in APL w/ PML-RAR fusion (suppresses DNA txn at normal retinoic acid levels–>accumulation promyelocytes/differentiation block)

Differentiation syndrome.

  • Fever, leukocytosis, dyspnea, weight gain, diffuse pulmonary infiltrates, and pleural and/or pericardial effusions.
  • Observed with WBC > 10,000/mm3. Usually observed during the first month of therapy but may follow the initial drug dose.
60
Q

Arsenic Trioxide

A

Induces differentiation of APL cells by degrading the chimeric PML/RAR-α protein, resulting in release of the maturation block.

ADE: Differentiation syndrome, QT prolongation

61
Q

thalidomide

A

induce apoptosis, enhance T-cell and NK cell cytotoxicity, inhibit angiogenesis

Used for multiple myeloma

ADE: sedation, constipation, rash, neuropathy

  • restricted distribution system, teratogen
62
Q

lenalidomide

A

induce apoptosis, enhance T-cell and NK cell cytotoxicity, inhibit angiogenesis

Used for multiple myeloma

ADE: marrow suppression, thromboembolism, restricted distribution system, teratogen

63
Q

pomalidomide

A

induce apoptosis, enhance T-cell and NK cell cytotoxicity, inhibit angiogenesis

Used for multiple myeloma

ADE: restricted distribution system, teratogen

64
Q

Bortezomin

A

inhibits proteasome–>prevents degradation of pro-apoptotic proteins

highly active in MM

toxicities: neuropathy and thrombocytopenia

65
Q

immediate effects of chemotherapy

A

within hours to days after chem/RT

nausea, vomiting

flushing, immediate hypersensitivity

hemorrhagic cystitis (cyclophosphosphamide)

fever, chills

66
Q

early effects of chemo therapy

A

days to weeks after Chemo/RT

corresponds to rapidly proliferating cell compartments

hematopoeitic: dec. WBC, platelets

stomatitis

cerebellar ataxia (5-FU)

alopecia

pancreatitis (L-asparaginase)

67
Q

delayed effects of chemotherapy

A

observed wks to months after therapy

anemia (lifespan RBC 120d)

pulmonary fibrosis (bleomycin, busulfan)

cardiotoxicity (anthracyclines: doxorubicin)

SIADH (cyclophosphamide, vincristine)

hepatocellular damage

cholestatic jaundice (6-MP)

azoospermia

68
Q

late effects of chemotherapy

A

occur months or years after therapy

sterility and hypogonadism

endocrinopathies

second malignancies

encephelopathy

69
Q

Grading of toxicity

A

NCI: CTEP, RTOG; other

Grades 1-4, with 4 the worse

1: no interference w/ activity
2: interferes w/ activity: outpt treatment

3,4: may require hospitalization, sig. change in functional status

5: fatal

CTC: common toxicity criteria (standard use protocol)

70
Q

Toxicity: hypersensitivity

A

I: bronchospasm, wheezing, agitation, rash, angioedema; starts in minutes (esp. monoclonal antibodies)

II: delayed, includes hemolytic anemia

III: interstitial penumonitis, vasculitis (eg. methotrexate)

Drugs:

  • L-asparaginase
  • paclitaxel, docetaxel (premedicate w/ steroids, anti-HI, H2)
  • procarbazine
  • teniposide

uncommon drugs:

  • anthracyclines, bleomycin
  • carboplatin, cisplatin
  • cyclophosphadmide, chlorambucil, busulfate
  • cytarabine, gemcitibine
  • interferosn
  • vicas, etc
71
Q

Toxicity: nausea and vomiting

A

Mechanism:

  • chemoreceptor trigger zone: CNS
  • cerebral cortex: anticipatory
  • vestibular stimuli
  • vagal afferents
  • chemical and physical stimuli to GI tract
  • metabolic (hypercalcemia hepatic, renal failure, DKA etc)**causes other than chemo itself

Anti-emetics:

  • 5-HT3 receptor antagonists
  • antihistamines
  • corticosteroids
  • cannabinoids
  • benzodiazepines
  • phenothiazines (compazine)
  • substituted benzamides (reglan)
  • substance P (NK1) antagonist (for delayed nausea and vomiting)
72
Q

toxicity: mucositis

A

early complication

both radiation and chemo

erythema,early ulceration–>confluent ulceration and pseudomembranes

assoc. w/ pain

bacterial and fungal superinfection common

73
Q

toxicities: neuro

peripheral or central

A

peripheral neurotoxicity: motor or sensory neuropathy

  • taxanes
  • vincas (motor neuropathy)
  • platinum based compounds

central neurotoxicity:

  • ifosphamide
  • high dose methotrexate
  • fluorouracil
  • procarbazine
  • ara-C (cerebellar)
  • fludarabine
74
Q

toxicities: nephrotoxicity

A

cisplatin, gallium, high dose methotrexate

azactidine, streptozocin

occasional: fludarabine, mitomycin, interferons, lomustine
uncommon: carboplatin, low dose methotrexate

*nephrotoxicity and ototoxicity go together

75
Q

toxicities: cystitis

A

early or late

suprapubic pain, dysuria, urgency, hematuria

cyclophosphamide, ifosphamide

mesna (sodium 2 mercaptoethanol sulfonate)–>prevent hemorrhagic cystitis

76
Q

toxicities: pulmonary

A

drug or radiation

radiation: varies w/ total dose, number of fractions, volume irradiated

bleomycin (dose dependent, early idiosyncratic rxns, toxicity enhanced by inc. FiO2 and concurrent RT)

Other drugs:

  • busulfan, cyclophosphamide, chloambucol
  • nitrosureas
  • bleomycin, mitomycin
  • methotrexate, ara-C, mercaptopurine
  • procarbazine, etoposide, retinoic acid

MOA:

  • free radical formation, activation of inflammation
  • upregulate collagen formation by fibroblasts
  • cytokines (IL1, TGFbeta etc)

Pathology:

  • vascular damage
  • desquamation of type 1 pneumocytes
  • delamellation and proliferation of type II pneumocytes
  • mononuclear cell infiltration

Sx:

  • dyspnea
  • cough, fatigue, fever
  • chest pain, rarely
  • hemoptysis, uncommon

Acute:

  • taxols (bronchospasm, anaphylaxis or pulmonary edema)
  • ATRA (respiratory distress, mediated by marginating leukemia cells in pulmonary circulation, w/ cytokine release and neutrophil migration, prevented by steroids)

Radiology:

  • reticulonodular pattern
  • pleural effusions
  • nodules
77
Q

toxicity: cardiotoxicity

A

anthracyclin (doxorubicin/adriamycin)

  • dose and schedule dependent
  • preexisting cardiac disease inc. risk
  • older age inc. risk
  • concurrent radiation to heart, cyclophosphamide inc. risk

Acute toxicity: uncommon–myopericarditis, arrhythmias, effusion

subacute: classic–up to 30months, inc. tachycardia, fatigue, pulmonary edema and CHF
late: 5+ years after anthracycline

late decompensation in those who recovered (systolic function abnormality, arrythmias and death)

mechanism:

  • mitochondrial injury
  • depletion ATP and phosphocreatine
  • depression contractility
  • free radical formation, lipid peroxidation

monitoring/prevention: baseline evaluation prior to anthracyclines (EKG, ejection fraction, biopsy)

Other agents:

  • cyclophosphamide and ifosphamide (only high doses)
  • paclitaxel: arrythmias, sinus bradycardia (infrequent)
  • vincristine and vinblastine: rare autonomic dysfx
  • mitomycin: enhances cardiotoxicity
  • 5-FU: infrequent-pain, atrial arrythmia, ventricular dysfx, rare cardiac failure, coronary artery spasm. silent ischemic changes w/ continuous infusion
  • traztuzumab: herceptin
78
Q

toxicities:

bevacizumab

erlotinib, cetuximab

A

angiogenesist inhibitors: bevacizumab:

  • hypertension, proteinuria, inc. bleeding, clottting, bowel perforation

EGFR inhibitors: erlotinib, cetuximab:

  • folliculitis, diarrhea, interstitial pulmonary fibrosis
79
Q

toxicity: acute endocrine effects

A

early hypothyroidism: pazopanib

autoimmune: ipilumumab, T cell activation (diarrhea, thyroid)
hyperglycemia: steroids, pazopanib

80
Q

late endocrine effects

A

hypothyroidism after radiation therapy to neck and chest areas

hypopituitarism as late effect of radiation therapy

reproductive failure after either chemo or RT

  • accelerated menopause in women (longer time for osteoporosis, pyschosocial, hormonal manipulation)
  • sterility and azoospermia in men
  • aklyating agents most likely to cause this
  • antimitotic agents have reversible effects on reproduction
81
Q

toxicity: second malignancy

A

continued exposure to carcinogen

underlying germ line abnormality or susceptibility

related to primary tumor

radiation induced leukemia: atomic bomb, nuclear accident

breast cancer following low dose radiation, esp. in childhood or adolescence

radiation and lung cancer: minimal

alkylating agents: risk of leukemia and myelodysplasia

topoisomerase II inhibitors: leukemia risk

82
Q
A

Heme/onc (5 decks)

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