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Heme Pharm > Drugs for Lymphoma/Leukemia > Flashcards

Drugs for Lymphoma/Leukemia Flashcards

1
Q

An analog of 2’-deoxycytidine

A

Cytarabine (antimetabolite, a cytidine analog)

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2
Q

Stem cells, pro-B cells, and antibody-producing plasma cells do not express CD20 and, therefore, are not affected by 1)

A

1) rituximab

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3
Q

Mechanism of Action: Have lympholytic effects and are able to suppress mitosis in the lymphocytes

A

Glucocorticoids Prednisone, Dexamethasone

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4
Q

Asparaginase Resistance arises through induction of 1) in tumor cells

A

1) asparagine synthetase

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5
Q

Adverse reactions Neurotoxicity: Nausea and vomiting; 1) can cause more severe toxicity including altered mental status, coma, seizures

A

Cyclophosphamide 1)ifosfamide

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6
Q

All histologic subtypes of Hodgkin lymphoma are treated in a similar fashion with the drug combination, (1)).

A

1)ABVD (doxorubicin [Adriamycin], bleomycin, vinblastine, and dacarbazine)

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7
Q

Mechanism of resistance: Increased intracellular concentrations of nucleophilic substances, e.g., glutathione, which can conjugate and detoxify electrophilic intermediates

A

Bleomycin; Cyclophosphamide

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8
Q

Chronic Myeloid leukemia (CML) treatment:

A

Imatinib

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9
Q

competitively binds to the ATP binding site on the bcr-abl which inhibits phosphorylation of proteins involved in CML clone proliferation

A

Tyrosine kinase inhibitor - Imatinib

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10
Q

must be activated by conversion to the 5’-monophosphate nucleotide and then to the diphosphate and triphosphate; triphosphate form competes with the physiological substrate deoxycytidine 5’-triphosphate (dCTP) for incorporation into DNA by DNA polymerases. The incorporated cytarabine residue is a potent inhibitor of DNA polymerase, both in replication and repair.

A

Cytarabine

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11
Q

Adverse reactions (a) Nausea, vomiting, edema (ankles and periorbital tissues), and muscle cramps (b) Neutropenia and thrombocytopenia

A

Imatinib

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12
Q

Bleomycin moa: binds 1) and chelates 2), leading to formation of free radicals that cause 3) break

A

1) DNA 2) iron 3) single- and double-strand DNA

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13
Q

APL is uniquely characterized by the t(15;17) translocation that fuses the 1) on chromosome 15 to the 2) gene on chromosome 17. Tretinoin induces promyelocyte differentiation and maturation. The use of concurrent tretinoin plus daunorubicin for induction

A

1) PML gene 2) retinoic acid receptor-alpha (RAR-α)

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14
Q

Adverse reactions: Cutaneous toxicity: Hyperpigmentation, hyperkeratosis, erythema, and ulcerations over the elbows, knuckles, and other pressure areas

A

Bleomycin

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15
Q

drugs are specific for the S phase of the cell cycle

A

Cytarabine

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16
Q

a/E Severe local vesicant action and tissue necrosis upon extravasation

A

anthracyclines (Doxorubicin; Daunorubucin)

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17
Q

Myelosuppression

A

methotrexate

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18
Q

an effective chain terminator when incorporated into DNA and the incorporation of fludarabine into RNA inhibits RNA function, RNA processing, and mRNA translation

A

Fludarabine

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19
Q

Mercaptopurine MOA: biotransformed into 1) which inhibit p. synthetase and p. aminotransferase, two enzymes critical for the synthesis of 2), which in turn is an essential step in 3); The 1) also causes DNA damage upon intercalation

A

1) false purine nucleotides 2) phosphoribosylamine 3) purine biosynthesis

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20
Q

MOA -Converted to the active triphosphate derivative; inhibits DNA polymerase, DNA primase, DNA ligase, and ribonucleotide reductase, and is incorporated into DNA and RNA. Stops DNA synthesis and RNA function, RNA processing, and mRNA translation

A

Fludarabine

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21
Q

What is dexrazoxane

A

cardioprotective iron-chelating agent; used to prevent cardiac toxicity with anthracycline use;

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22
Q

Resistance occurs due to decreased activation of the prodrug

A

Mercaptopurine (antimetabolite, purine analog)

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23
Q

How is cardiac toxicity caused by anthracyclines prevented”

A

prevented by concomitant use of dexrazoxane, a cardioprotective iron-chelating agent.

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24
Q

leads to a decrease in the synthesis of 1), which is a one carbon unit carrier. These one carbon units are used in the synthesis of 2) which in turn are essential for the synthesis of DNA and RNA

A

1) tetrahydrofolate 2) purines and pyrimidines refers to methotrexate

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25
Q

Vinca alkaloids MOA bind 1) blocking its ability to polymerize with α-tubulin into 2) . In the absence of an intact mitotic spindle, duplicated chromosomes cannot align along the division plate. Cells blocked in mitosis undergo 3).

A

1) β-tubulin 2 microtubules 3) apoptosis

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26
Q

chimeric (mouse-human) monoclonal antibody (b) Binds to the CD20 antigen on the surface of pre-B cells and mature B cells, resulting in the depletion of B cells from peripheral blood, lymph nodes, and bone marrow

A

Biologicals - Rituximab

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27
Q

The bcr-abl fusion gene of the Philadelphia chromosome encodes for a 1) that is involved in both the increased proliferation of the CML clone and the reduction in FAS-mediated apoptosis

A

1) mutant tyrosine kinase

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28
Q

Adverse reactions (a) Myelosuppression is a major dose-limiting complication

A

anthracyclines (Doxorubicin; Daunorubucin)

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29
Q

Mechanisms of resistance: P-glycoprotein-mediated multi-drug resistance which decreases drug accumulation within tumor cells

A

anthracyclines (Doxorubicin; Daunorubucin)

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30
Q

The 1) is expressed on a high percentage of CLL cells. Rituximab is a chimeric human-murine anti-CD20 monoclonal antibody but it is not indicated as a single agent therapy

A

1) CD20 surface antigen

31
Q

folinic acid (leucovorin) by-pass the 1) step in tetrahydrofolate synthesis. This agent can rescue host cells while cancer cells are less affected

A

1) dihydrofolate reductase

32
Q

Asparaginase catalyzes the hydrolysis of circulating 1) to 2) depriving malignant cells of the asparagine necessary for 3) synthesis, leading to cell death

A

1) asparagine 2) aspartic acid and ammonia 3) protein

33
Q

The drug also is degraded by a specific hydrolase found in various normal tissues including the liver. The hydrolase activity is low in the skin and lungs and drug concentrations are high in these sites which contributes to toxicity;

A

Bleomycin

34
Q

biotransformed to polyglutamate 1) which in turn competitively inhibits dihydrofolate reductase, the enzyme responsible for the reduction of dihydrofolate to tetrahydrofolate

A

1) methotrexate

35
Q

Drug interactions Concurrent use of drugs that reduce renal blood flow (e.g., nonsteroidal antiinflammatory agents), that are nephrotoxic (e.g., cisplatin), or that are weak organic acids (e.g., aspirin or piperacillin ) can delay drug excretion and lead to severe myelosuppression

A

methotrexate

36
Q

prodrug which is converted in the liver to the active compound, phosphoramide mustard. This drug has a highly reactive alkyl groups that forms covalent bonds between guanines resulting in cross-linking between two DNA strands. DNA cannot be replicated resulting in cell death

A

Cyclophosphamide

37
Q

1), a metabolite of cyclophosphamide and ifosfamide, causes 2). This can be prevented by coadministration of 3) which conjugates acrolein

A

1) Acrolein 2) hemorrhagic cystitis 3) mesna (2-mercaptoethanesulfonate)

38
Q

Adverse reactions: Peripheral neuropathy

A

Fludarabine

39
Q

Adverse reactions: Severe injury may occur as a result of local toxic extravasation

A

Vincristine and Vinblastine

40
Q

Anthracyclines can form 1), which in turn can react with oxygen to produce 2). These can generate both hydrogen peroxide and hydroxyl radicals (·OH), which attack DNA and oxidize DNA bases. The production of free radicals is significantly stimulated by the interaction of doxorubicin with 3).

A

1) radical intermediates 2) superoxide anion radicals 3) iron

41
Q

A/E Gastrointestinal disturbances, stomatitis, conjunctivitis, reversible hepatic enzyme elevations, noncardiogenic pulmonary edema, and dermatitis.

A

Cytarabine

42
Q

Mechanisms of resistance: Increased rates of metabolism of active forms to its inactive form

A

Cyclophosphamide

43
Q

A/E- Urotoxic: Acrolein, a metabolite of 1), causes hemorrhagic cystitis.

A

1) cyclophosphamide and ifosfamide

44
Q

Adverse reactions: Cardiac toxicity manifested as ECG changes acutely and cardiomyopathy w/ long term use:

A

anthracyclines (Doxorubicin; Daunorubucin)

45
Q

what is folinic acid aka leucovorin

A

Counteracts myelosuppression in Methotrexate use;

46
Q

Asparaginase AE: Inhibition of protein synthesis in normal tissues can lead to 1), clotting abnormalities due to deficient clotting factors, and 2)

A

1) hyperglycemia due to insulin deficiency 2) hypoalbuminemia

47
Q

binds DNA and chelates iron, leading to formation of free radicals that cause single- and double-strand DNA breaks

A

Bleomycin

48
Q

Resistance results from mutations in the kinase domain rendering it less sensitive

A

Imatinib

49
Q

Adverse reactions (a) Myelosuppression

A

Cyclophosphamide

50
Q

Adverse reactions (a) Myelosuppression, nausea and vomiting, chills and fever, malaise, anorexia, and weakness

A

Fludarabine

51
Q

form a ternary complex with topoisomerase II and DNA.

A

Doxorubicin (a.k.a. hydroxydaunorubicin), daunorubicin:

52
Q

Mechanisms of resistance: Mutation or decreased expression of topoisomerase II

A

anthracyclines (Doxorubicin; Daunorubucin)

53
Q

Adverse effects (a) Potent myelosuppressive agent capable of producing acute, severe leukopenia, thrombocytopenia, and anemia

A

Cytarabine

54
Q

biotransformed into false purine nucleotides which inhibit phosphoribosylpyrophosphate synthetase and phosphoribosylpyrophosphate aminotransferase, two enzymes critical for the synthesis of phosphoribosylamine, which in turn is an essential step in purine biosynthesis

A

Mercaptopurine (antimetabolite, purine analog)

55
Q

Adverse reactions: Pulmonary toxicity; Begins with cough and rales progressing to fibrosis; may be reversible but patients die of this complication

A

Bleomycin

56
Q

Adverse effects (a) Antigenicity as a foreign protein-Hypersensitivity reactions can occur and may be fatal (b) Inhibition of protein synthesis in normal tissues which can lead to hyperglycemia due to insulin deficiency, clotting abnormalities due to deficient clotting factors, and hypoalbuminemia

A

Asparaginase

57
Q

bind β-tubulin blocking its ability to polymerize with α-tubulin into microtubules. In the absence of an intact mitotic spindle, duplicated chromosomes cannot align along the division plate. Cells blocked in mitosis undergo apoptosis.

A

Antimitotic drugs - Vincristine and vinblastine (vinca alkaloids)

58
Q

A/E Cerebellar toxicity, manifest as ataxia and slurred speech, and cerebral toxicity, including seizures, dementia, and coma, may follow intrathecal administration or high-dose systemic administration

A

Cytarabine

59
Q

Adverse reactions (a) Nausea and vomiting (b) Myelosuppression (c) Extravasation of the drug upon intravenous administration can cause severe pain and tissue damage

A

Dacarbazine

60
Q

A/E a) bone marrow depression- thrombocytopenia, granulocytopenia, anemia (b) Anorexia, nausea, vomiting

A

Mercaptopurine

61
Q

Adverse effects Acute infusion reactions, associated particularly with the first infusion, including fever, chills, urticaria, headache, bronchospasm, angioedema and hypotension

A

Biologicals - Rituximab

62
Q

cell-cycle-specific agents blocking cells in mitosis (M phase). Cell division is arrested in metaphase

A

Antimitotic drugs - Vincristine and vinblastine (vinca alkaloids)

63
Q

t(15;17) –> blocks maturation and differentiation b/c of 1); the fusion protein binds retinoids w/ much less affinity, lacks PML inhibitory function, and blocks the function of transcription factors which promote 2). Tretinoin activates the differentiation program and promotes degradation of the PML-RAR-fusion gene.

A

1) alterations of the RAR 2) myeloid differentiation.

64
Q

topoisomerase II function is essential for DNA replication and repair. Formation of the tripartite complex with 1) inhibits the re-ligation of the broken DNA strands, leading to 2)

A

1) anthracyclines (Doxorubicin; Daunorubucin) 2) apoptosis

65
Q

1) is one of the few malignancies that is typically curable, even in the advanced stages

A

1) Hodgkin lymphoma

66
Q

displaces the repressor, activating the differentiation program,and promoting degradation of the PML-RAR- fusion gene

A

Differentiating agents - Tretinoin

67
Q

Allopurinol inhibits xanthine oxidase, an enzyme responsible for degrading 1)—decrease the dose of 1)

A

1) mercaptopurine

68
Q

prodrug that is converted in the liver to MTIC which interrupts DNA replication by causing methylation of guanine

A

Dacarbazine

69
Q

a/E Mucositis

A

anthracyclines (Doxorubicin; Daunorubucin)

70
Q

Resistance occurs via Production of altered forms of DHFR that have decreased affinity for the inhibitor

A

methotrexate

71
Q

Doxorubicin; Daunorubucin a/e: Cardiac toxicity manifested as ECG changes acutely and cardiomyopathy with long term use. The drug accumulates in the heart which has low levels of defensive enzymes that convert 1) to less reactive compounds.1) cause the cardiac damage. This can be prevented by concomitant use of 2), a 3) agent

A

1) free radicals 2) dexrazoxane 3) cardioprotective iron-chelating

72
Q

Topoisomerase II is an ATP-dependent enzyme that binds to DNA and produces 1) at the 3’ phosphate backbone, allowing strand passage and uncoiling of supercoiled DNA. Following strand passage, topoisomerase II 2) the DNA strands

A

1) double-strand breaks 2) religates

73
Q

Adverse reactions i. Neurotoxicity manifested as numbness and tingling of the extremities and loss of deep tendon reflexes, and motor weakness (microtubules are important in nerve conduction and neurotransmission)

A

Antimitotic drugs - Vincristine and vinblastine (vinca alkaloids)

Heme Pharm (13 decks)

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