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Pharm > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

Define primary chemotherapy?

A

Chemotherapy indicated when neoplasms are disseminated and not amenable to surgery

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2
Q

Define adjuvant chemotherapy?

A

Chemotherapy used to attack micrometastases following surgery and radiation

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3
Q

Define neoadjuvant chemotherapy?

A

Chemotherapy given prior to surgery to shrink the cancer

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4
Q

Methotrexate

A

MOA: inhibits dihydrofolate reductase > decrease synthesis of dTMP and purine nucleotides > decrease DNA, RNA, protein synthesis > cell death

AE: common is stomatits, myelosuppression, alopecia, nausea, and vomiting. Others are renal damage, hepatic fibrosis/cirrhosis, pneumonitis, and neurological toxicites

HL: metabolized by folylpolyglutamate synthase (FPGS) to polygulamates (MTX-PGs). Given in combination with Leucovorin which is N5-formyl-THF which provides normal tissue with reduced folate

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5
Q

What are the two purine analogs?

A

6-mercaptopurine and 6-thioguanine

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6
Q

6-mercaptopurine

A

MOA: convereted to thio-IMP by HGPRT > inhibits first step of de novo purine ring biosynthesis and blocks formation of AMP/GMP from IMP > dysfunctional RNA and DNA > cell death

AE: nausea, vomiting, diarrhea, bone marrow supression, and hepatotoxicity

HL: metabolized by xanathine oxidase to thiouric acid and by thiopuring methyltransferase (TPMT). If allopurinol is given with reduce hyperuricemia dose of 6-MP must be reduced because allopurinol is xanthine oxidase inhibitor.

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7
Q

6-thioguanine

A

MOA: converted to nucleotide > inhibits purine synthesis and the phosphorylation of GMP to GDP

AE: nausea, vomiting, diarrhea, bone marrow suppression, hepatotoxicity

HL: allopurinol does not potentiate 6-TG action because very little is metabolized to thiouric acid. Metabolized by thiopuring methyltransferase (TPMT)

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8
Q

What are the 3 pyrimidine analogs?

A

5-fluorouracil, Capecitabine, and Cytarabine

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9
Q

5-fluorouracil

A

MOA: converted to 5-FdUMP and 5-FUTP > inhibits thymidylate synthase > thymineless death

AE: nause vomiting, alopecia, bone marrow depression and hand-foot syndrome

HL: combined with leucovorin for colorectal cancer because increasing levels of N5,N10-methylene-THF potentiates activity

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10
Q

Capecitabine

A

MOA: same as 5-FU

AE: same as 5-FU

HL:

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11
Q

Cytarabine (ARA-C)

A

MOA: analog of deoxycytidine > phosphorylated to triphosphate > incorporated into DNA > inhibits DNA polymerase

AE:

HL:

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12
Q

Anthracyclines (Doxorubicin and Daunorubicin)

A

MOA: inhibition of topoisomerase II, intercalation in DNA with consequent blockade of DNA/RNA synthesis and strand breakage, binding to cell membranes to alter fluidity/ion transport, generation of free radicals

AE: myelosuppression, cardiotoxicity

HL: dexrazoxane can redue the cardiotoxicity

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13
Q

Bleomycin

A

MOA: mixture of glycopeptides > DNA-bleomycin-Fe2+ > oxidation to bleomycin-Fe3+ > reacts with O2 forming free radicals > strand breakdown

AE: very little myelosuppression, pulmonary toxicity (pneumonitis, fibrosis)

HL: cell-cycle specific with arrest cells in G2 phase

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14
Q

What are the different types of alkylating agents?

A

Nitrogen mustards, nitrosoureas, other alkylating agents, and platinum coordination complexes

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15
Q

What are the 3 nitrogen mustards?

A

Mechlorethamine, cyclophasphamide, and melphalan

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16
Q

Mechlorethamine

A

MOA: alkyating > cell death

AE: severe nausea/vomiting, severe bone marrow depression, alopecia, immunosuppression,

HL: powerful vesicant so only given by IV

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17
Q

Cyclophosphamide

A

MOA: alkylating > cell death

AE: nasuea/vomiting, bone marrow depression, hemorrhagic cystitis, alopecia, and sterility

HL: its a prodrug, most widely used, and mesna + fluid intake is taken to prevent acrolein buildup leading to hemorrhagic cystitis

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18
Q

Melphalan

A

MOA: alkylating agent > cell death

AE: bone marrow suppression

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19
Q

What are the 2 nitrosoureas?

A

Carmustine and lomustine

20
Q

Nitrosoureas

A

MOA: alkylation > cell death

HL: very lipophilic, cross BBB, treatment of brain tumors

21
Q

What the the 3 other alkylating agents?

A

Busulfan, dacarbazine, and procarbazine

22
Q

Busulfan

A

MOA: alkylating

AE: myelosuppression and pulmonary fibrosis

23
Q

Dacarbazine

A

MOA: methylating agent after activation in liver

AE: nausea/vomiting, myelosuppression mild to moderate

HL: given IV

24
Q

Procarbazine

A

MOA: converted by liver P450 to alkylating metabolites

AE: bone marrow depression, nausea/vomiting, weak MAO inhibitor, disulfiram-like reaction, mutagenic/teratogenic

25
Q

What are the 2 platinum coordintation complexes?

A

Crisplatin and carboplatin

26
Q

Crisplatin

A

MOA: inhibit DNA synthesis and bind DNA through cross-links

AE: myelosuppression mild to moderate, nausea/vomiting, ototoxicity, peripheral neuropathy, nephrotoxicity

HL: Amifostine reduced the renal toxicity

27
Q

Carboplatin

A

MOA: inhibit DNA synthesis and bind DNA through cross-links

AE: less nausea, neurotoxicity, ototoxicity, and nephrotoxicity than cisplatin but dose limiting toxicity is myelosuppression

28
Q

What are the 2 type of microtubule inhibitors and what 2 drugs belong to each group?

A

Vinca alkaloids: vincristine and vinblastine

Taxanes: paclitaxel and docetaxel

29
Q

Vinca Alkaloids

A

MOA: bind beta-tubulin > inhibit ability to polymerize into microtubules > apoptosis

AE: vincristine is peripheral neuropath, bone marrow suppression mild, and alopecia. Vinblastine is myelosuppression as dose limiting

HL: mitotic arrest in metaphase

30
Q

Taxanes

A

MOA: bind beta-tubulin subunit of microtubules > promote microtubule polymerization

AE: paclitaxel is hypersensitivity, myelosuppression, peripheral neuropathy, alopecia. Docetaxel is myelosupression, peripheral neuropathy, fluid retention, alopecia, and mucositis.

HL: hypersensitivity reduced by dexamethaone, diphenhydramine, and an H2 blocker. Also for docetaxel dexamethasone is required to prevent fluid retention.

31
Q

Etoposide

A

MOA: inhibits topoisomerase II > DNA damage by strand breakage

32
Q

Camptothecins (topotecan and irinotecan)

A

MOA: inhibit topoisomerase I > DNA damage

33
Q

What are the 3 types of hormonal agents?

A

Glucocorticoids, estrogen inhibitors, androgen inhibitors

34
Q

Prednisone

A

MOA: glucocorticoids are lympholytic and supress mitosis in lymphocytes

HL: used for acute leukemia and malignant lymphomas

35
Q

What are the 3 types of estrogen inhibitors?

A

Selective Estrogen-Receptor Modulators (SERMs), Selective Estrogen-Receptor Downregulators (SERDs), and Aromatase Inhibitors (AIs)

36
Q

Tamoxifen

A

MOA: bind estrogen receptors and act as agonist or antagonist depending on tissue

HL: antagonist on receptor-positive breast cancer

37
Q

Raloxifene

A

MOA: antiestrogen in the uterus and breast while promoting estrogenic effects in bone to inhibit resorption.

HL: prevention of postmenopausal osteoporsis and prophylaxis of breast cancer

38
Q

Fulvestrant

A

MOA: binds estrogen receptor > inhibits dimerization > increases its degredation

HL: estrogen receptor mediated transcription is abolished

39
Q

Anastrozole & Letrozole

A

MOA: nonsteroidal reversible competitive inhibitor of aromatase

40
Q

Exemestane

A

MOA: steroidal and irreversible inhibitor of aromatase

41
Q

What are the two groups of androgen inhibitors?

A

Gonadotropin-releasing hormone agonists and androgen receptor blockers

42
Q

Goserelin and Leuprolide

A

MOA: GnRh agonist > initial surge of LH/FSH levels > inhibition of gonadotropin release > testosterone drop to 10% in a month

HL: initial surge can be conteracted by concurrent administration of flutamide for 2-4 weeks

43
Q

Flutamide

A

MOA: metabolized to active metabolite that acts as competitive antagonist of androgen receptor prevent translocation to nucleus

HL: synthetic nonsteroidal antiandrogen

44
Q

What are the 5 inhibtors of receptor tyrosine kinases and what does each do?

A

Lapatinib: inhibitor of EGFR and ErbB2 tyrosine kinase

Erlotinib: inhibitor of EGFR tyrosine kinase

Gefitinib: inhibitor of EGFR tyrosine kinase

Imatinib: inhibitor of the tyrosine kinase of Bcr-Abl

Trastuzumab: monoclonal antibody against ErbB2

45
Q

Asparaginase

A

MOA: hydrolyzing sereum asparagine > depriving cell of asparagine necessary for protien synthesis > cell death

AE: hypersensitivity, decrease clotting factors, liver abnormalities, ammonia toxicity (pancreatitis, seizures, coma)

46
Q

Hydroxyurea

A

MOA: inhibits ribonucleotide reductase > depletion of deoxynucleoside triphosphate pools > inhibited DNA synthesis > kills cells in S phase

47
Q

Interferon alpha

A

approved for hair cell leukemia, chronic myelogenous leukemia (CML), malignant melanoma, and Kaposi’s sarcoma

Pharm (14 decks)

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