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CMBM exam 5 > Anti-neoplastic drugs > Flashcards

Anti-neoplastic drugs Flashcards

1
Q

What does the therapeutic window for a anticancer drug look like?

A

Very small

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2
Q

When you combine cancer drug what should NOT be done?

A

Should not combine ones with the same actions and the same toxicities

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3
Q

Why are multiple cycles of an anti cancer drug needed?

A

Only kills 99% of the cells and the 1% can grow back quickly

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4
Q

Which cells are the most susceptible to chemotherapy?

A

Rapidly growing cells

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5
Q

Which cancer drugs enter at the M phase of the cell cycle?

A

Vincristine
Vinblastine
Vinorelbine
Paclitaxel

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6
Q

Which cancer drugs enter at the S phase of the cell cycle?

A

Cytarabine
6-mercaptopurine
Methotrexate

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7
Q

What are the nitrogen mustards? *

A

Mechlorethamine
Cyclophosphamide
Ifosfamide

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8
Q

What are the platinum complexes? *

A

Cisplatin

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9
Q

What are the nitrosoureas?

A

Lomustine

Carmustine

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10
Q

What are the triazenes?

A

Dacarbazine

Temozolomiden

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11
Q

What are the methylhydrazines?

A

Procarbazine

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12
Q

What are the alkyl sulfonate? *

A

Busulfan

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13
Q

What does cross linked DNA do?

A

Interferes with DNA replication and causes cell cycle arrest

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14
Q

What chemotherapeutic drugs are alkylating agents?

A 
Nitrogen mustards
Platinum complexes
Nitrosoureas
Triazenes
Methylhydrazine
Alkyl sulfonate
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15
Q

What is the mechanism of action for alkylating agents? *

A

Cross links the DNA

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16
Q

Mechloresthamine (Mustargen) *

A

Most reactive nitrogen mustard
Pharm: unstable, given IV immediately after being made up
Toxic: N&V, bone marrow, tissue damage w/ extravesation

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17
Q

Cyclophosphamide (Cytoxan, Neosar) *

A

Pharm: well absorbed orally, prodrug which must be converted by liver cytochrome P450 to active metabolite
Toxic: N&V, cardiotoxic, hemorrhagic cystitis, bladder burn, hematuria, bone marrow toxic

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18
Q

What is the mechanism of platinum complexes? *

A

Covalent crosslink with GG base pairs to bend DNA

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19
Q

Cisplatin (Platinol): Pharmacology *

A

IV, 90% bound to plasma protein, concentrates in liver, kidney, intestine, ovary and excreted in urine

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20
Q

Cisplatin (Platinol): Toxicity *

A

N&V, hypersensitivity rashes, renal damage (hydrate to stop), ototoxicity w/ high frequency hearing loss + tinnitus, peripheral sensory neuropathy and bone marrow depression

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21
Q

Busulfan (Busulfex, Myleran) *

A

Pharm: Oral, half life 2/3 hrs

* Toxicity: N&V, bone marrow depression (stem cells), pulmonary infiltrates and fibrosis

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22
Q

What is the mechanism of antimetabolites?

A

Block formation of DNA
Form abnormal DNA
Cell cycle dependent
Inhibit protein synthesis

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23
Q

What are the antimetabolites?

A 
Methotrexate, Asparaginase
Fluorouracil, 
Capecitabine, 
Cytarabine, 
Mercaptopurine
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24
Q

What is the mechanism for methotrexate?

A

Analog of floic acid
Competitive inhibitor of dihydrofolate reducatse
Blocks dTMP synth which is required for DNA synth
Inhibits the folate-dependent enzymes of de novo purine and thymidylate synth

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25
Methotrexate *
Pharm: Oral, IV, IM, Intrathecally, majority excreted unchange in urine * Tox: Alopecia, N&V, diarrhae, fever, hepatic necrosis, hypersenitivity rxns, oral + Gi ulcers, bone marrow depression, pulmonary infiltrates and fibrosis
26
What is the mechanism for fluorouracil?
Converted to fraudulent F-dUMP Fraud F-dUMP forms a covalent complex with thymidylate synthase and methylene tetrahydrofolate Results in inhibition of DNA synth
27
Fluorouracil
Pharm: IV, distributes through body and brain, metabolized in liver, short half life (10-15 min) * Tox: severe ulceration of oral + Gi mucosa, N&V, diarrhea, alopecia, bone marrow depression
28
Capecitabine (Xeloda)
Pharm: converted to 5-FU by an thymidine phosphorylase which is highly expressed in solid tumors, oral admin
29
What is the mechanism of Cytarabine (cytosine arabinoside)?
2'-deoxycytidine analog; phosphorylated to aracytidine triphosphate 2'-hydroxyl trans tp 3'hydroxyl hunders rotation of base and inhibits DNA chain elongation Inhibits DNA pol
30
How does DNA chain elongation work?
The OH group of the 3' carbon of the sugar of one nucleotide forms an ester bond to the phosphate of another nucelotide eliminating a molecule of water Next nucleotide added to 3' end
31
Cytarabine (ctosine arabinoside)
Pharm: IV, rapidly inactivated by cytidine deaminase in GI and liver * Tox: bone marrow depression, oral ulcers, hepatic damage, N&V, diarrhea, anaphylaxis, fever, pulmonary edema, high does = sudden respiratory distress and CNS toxicity
32
What is the clinical use of cytarabine?
Acute myelocytic leukemia (AML) Lymphoblastic leukemia (ALL) Chronic myelogenous leukemia (CML)
33
What is the mechanism of 6-mercaptopurine?
Converted to 6-mercaptopurine ribose phosphate; inhibits purine (guanine) synth Triphosphate form can be incorperated into DNA resulting in DNA strands and breaks Used for leukemia in children
34
6-mercaptopurine
* Pharm: oral bioavailability - 5-37%, IV half life 50 min, metabolized in liver * Tox: bone marrow depression, N&V (25%), hepatic enzyme elevate (33%)
35
If a pt is receiving oral doses of 6-mercaptopurine how much should it be reduced to if the pt is also receiving Xanthine oxidase inhibitors (allopurinol)? *
75%
36
What are the thymine pyrimidine antimetabolites?
Fluorouracil (5-FU), capecitabine, floxuridine, idoxuridine
37
What are the cytosine pyrimidine antimetabolites?
Cytarabine (Ara-C, cytosine arabinoside), 5-azacytidine, decitabine, gemcitabine
38
What are the guanine purine antimetabolites?
6-mercaptopurine, azathioprine
39
What are the adenine purine antimetabolites?
Fludarabine, cladrabine, pentostatin
40
What is a purine antimetabolite (non-specified)?
Methotrexate
41
What are the three phosporylation events of a nucleoside analog?
First is rate-limiting nucleoside kinase Triphosphorylated analongue can incorporate into DNA/RNA and/or inhibit enzymes Active nucleoside analogues catabolized by 5'-nucleotidase and deaminase
42
What is the mechanism of Asoarginase Erwinia chrysanthemi (Erwinaze)? *
Hydrolyze asparagine to aspartic acid and ammonia Some lymphoid malignancies require L-asparagine from plasma Inhibits protein synth
43
Asoarginase Erwinia chrysanthemi (Erwinaze)
Pharm: IV | * Tox: risk of anaphylaxis, minimal effect on bone marrow and GI mucous, hyperglycemia, clotting deficiency
44
What is the clinical use for Asoarginase Erwinia chrysanthemi (Erwinaze)?
Acute lymphoblastic leukemia
45
Microtubule inhibitors; taxanes
Paclitaxel | Docetaxel
46
What is the shared mechanism of paclitaxel and docetaxel? *
Taxanes stabilize or freeze polymerized microtubules | Block mitosis metaphase arrest
47
Paclitaxel and docetaxel
Pharm: IV, metabolized in liver | * Tox: bone marrow toxicity, peripheral sensory neuropathy (dose limited) and hypersensitivity rxn
48
What is the mechanism of anthracycline antibiotics?
Intercalates into DNA and blocks the resealing action of topoisomerase II, generates free radical
49
What are the toxicities of anthracycline antibiotics?
Acute cardiac toxicity; arrhythmias ST & T wave alterations Chronic cardiac toxicity; cardiomyopathy leading to congestive heart failure unresponsive to digitals related to total cumulative dose Severe local tissue damage
50
Topoisomerase inhibitors; Anthracycline antibiotics
Doxorubicin
51
What are the topoisomerase inhibitors?
Anthracycline antibiotics Dactinomycin Etoposide Camptothecins
52
Topoisomerase inhibitors; Camptothecins
Irinotecan
53
What is the mechanism of topoismerase inhibitors?
Inhibits resealing of nicked DNA
54
What is the mechanism of doxorubicin? *
Intercalates into DNA and blocks the resealing action of topoisomerase II
55
Doxorubicin (Adriamycin)
Pharm: rapid infusion IV, distributes widely except to CNS, metabolized in liver and excreted in bile * Tox: N&V, red urine (not hematuria), severe local tissue damage with extravasation, diarrhea, fever, transient ECG changes, ventricular arrhythmia, cardiotoxicity
56
What is the mechanism for the toxicity of Doxorubicin?
Free radical damage: doxorubicin + Fe(+2) can generate hydroxyl radicals from peroxide Dexrazoxane: to protect from cardiotoxicity and treat extravastion from IV doxorubicin
57
What is the mechanism if irinotecan (camptosar)? *
Blocks the resealing action of topoisomerase I
58
Irinotecan (camptosar)
Pharm: IV * Tox: dose limiting myelosuppression and severe GI toxicity life-threatening Limited use of UGT1A1*28 polymorphism of Uridine disphoate
59
What is the therapeutic use of irinotecan?
Metastatic and recurrent colon cancer; small cell lung cancer
60
What is the free radical generator?
Bleomycin (blenoxane) - mixture of 2 cooper chelating glycopeptide antibodies
61
What is the mechanism of bleomycin? *
``` DNA-bleomycin-Fe(2+) complex forms DNA-bleomycin-Fe(2+) interacts with oxygen Forms superoxide (O2-) and hydroxyl free (OH-) radicals Radials produce DNA breaks (DNA fragmentation) DNA repair mechanism determine cytotoxicity ```
62
Bleomycin
Pharm: IV, subQ or IM, localized to skin, lymph, lung, lymphatic and peritoneum tissue, excreted in urine * Tox: N&V, fever, anaphlazis and phlebitis at injection site, degraded by hydrolysis which is low in lungs - pulmonary fibrosis, ulcers, hyperpigment
63
What are the hormone inhibitors?
Aromatase inhibitors | Hormone analogs
64
What are the aromatase inhibitors
Exemestane Letrozole Anastrozole
65
What is the mechanism of aromatase inhibitors?
Block the conversion of androgens to estrogen
66
What is the pharm and tox of aromtase inhibitors?
Oral | Musculoskeltal pain, headache, joint pain, hot flashes, fatigue, difficulty breathing, bone density, hot flashes
67
What is the therapeutic use for aromatase inhibitors?
Breast cancer, postmenopausal women
68
What are the hormone analogs?
Goserelin acetate | Megestrol acetate
69
What is the mechanism of goserelin acetate (Zoladex)?
Decapeptide analong of LHRH prolonged adminstration inhibits gonadotropin secretion = dec extradiol
70
What are the side effects of goserelin acetate?
Headache, hot flashes, emotional lability, depression, vaginitis
71
What is the therapeutic use for goserelin acetate?
Prostate cancer, advanced breat cancer in pre/peri-menopausal women
72
What is the mechanism for pamidronate disodium (Aredia)? *
Synthetic bisphosphate pamidronate | adsorb to calcium phosphate crystals in bone, blocks their dissolution by inhibiting osteoclast-mediated bone resorption
73
What are the side effects for pamidronate disodium?
Fever, severe joint, bone and muscle pain, seizure
74
What are the tyrosine kinase inhibitors?
Monoclonal antibodies | Chemical agents
75
What are the monoclonal antibodies?
Trastuzumab Bevacizumab Cetuximab Rituximab
76
What are the chemical agents?
Tamoxifen | Imatinib
77
Suffix for chimeric antibodies
-ximab
78
Suffix for humanized antibodies
-umab
79
Suffix for nonhuman host antibodies
-omab
80
What is the mechanism for monoclonal antibodies?
Antibody-dependent cell-mediated cyotoxicity Complement-mediated cytotoxicity Direct induction of apoptosis
81
What is the mechanism for trastuzumab? *
Recombinant DNA-derived humanized monoclonal antibody that recognizes the HER2 receptors that can be overexpressed on breast cancer cells HER2 receptor overexpression causes cells to grow, divide and multiply
82
What is the therapeutic use for trastuzumab? *
HER2 overexpressing metastatic breast cancer (25%)
83
What is the toxicity for trastuzumab? *
Weakening for the heart muscle, congestive heart failure, anemia
84
What is the mechanism for bevacizumab? *
Humanized monoloncal antibody that reconginzes vascualr-endothelial growth factor and inhibits ineteraction of VEGF with its receptors
85
What is the therapeutic use for bevacizumab? *
Treatment for metastatic colorectal cancer
86
What is the toxicity of bevacizumab? *
Proteinuria, hypertension, congestive heart failure, gastrointestinal perforations, pulmonary hemorrhage
87
What is the mechanism of cetuximab? *
Monoclonal antibody that binds to the epidermal growth factor receptor (EGFR or HER1) Block binding of epidermal growth factor and other ligands (TGF-a) to the receptor on normal and tumor cells Inhibits cell growth and induces apoptosis
88
What is cetuximab used for? *
Metastatic colorectal cancer | Resitricted in pts w/ wildtype KRAS
89
Cetuximab
Pharm: give IB every 2 weeks Tox: severe infusion rxn, acneiform rash, hypomagnesemia
90
What is the side effect of EGFR inhibitors?
Severe acneiform rash/eruption
91
What is Rituximab?
Chimeric human-mouse monoclonal that recognizes CD20
92
What is the mechanism of rituximab?
Complement-mediated cytoxicity Antibody dependent cell mediated cytotoicity Induction of apoptosis in malignant lymphoma cells
93
What is the clinical use for rituximab?
First line of treatment for CD20 B-cell malignancies Replased B-cell non-hodgkin's lymphoma Chronic lymphocytic leukemia
94
What are the side effects of rituximab? *
Infusion rxns, fever, chills, lymphopenia, infection, asthenia, hep B reactivation, leukoencephalopathy
95
What are immunoconjugates?
Attach radioisotope to monoclonal antibody (gamma or beta) Antibody binds target Cytotoxic ionizing radiation delivered to antigen expressing cells
96
What are the tyrosine kinase inhibitors?
``` Tamoxifen Lapatinib Imatinib Nilotininb Ponatinib ```
97
What is the mechanism of tamoxifen? *
Binds estrogen receptor | Competitive inhibitor of estradiol binding the estrogen receptor
98
Tamoxifen (nolvadex)
Pharm: oral, metabolized in liver w/ active metabolites (N-desmethyltamoxifen and trans 4-hydroxytamoxifen * Tox: N&V, hot flush, vag discharge, endometrial cancer, venous thrombosis + pulmonary emboli, stroke
99
What is the therapeutic use for tamoxifen? *
Estrogen-dependent breast cancer
100
What is the side effect to tamoxifen?
Reduced serum cholesterol and reduced maintenance of bone density
101
What is the mechanism of lapatinib? *
HER2 and EGFR (HER1) inhibitor
102
What is the mechanism of imantinib? *
Inhibitor of constitutively active Bcr-Abl tyrosine kinase (product of the Philadelphia chromosome) Blocks the ATP binding site on the kinase.
103
What is the mechanism of nilotinib (tasigna)? *
Inhibitor of Bcr-Abl tyrosine kinase Binds to and stabilizes the inactive conformation of the kinase domain of the Abl protein of the Bcr-Abl fusion protein Inhibits platelet-derived growth factor receptor (PDGF-R) and c-kit
104
What is the mechanism for ponatinib? *
Inhibits unmutated and all mutated forms of Bcr-Abl, including T315I, the highly drug therapy-resistant missense mutation of Bcr-Abl. Inhibits other tyrosine kinases associated with VEGFRs and FGFRs Inhibits the tyrosine kinase receptor TIE2 and FMS-related tyrosine kinase receptor-3 (Flt3)
105
Tretinoin toxicity *
“Retinoic acid syndrome” (fever, dyspnea, weight gain, pulmonary infiltrates, pleural or pericardial effusions), onset 2-21 days, potentially lethal
106
What is the target of tretinoin? *
Acute promyelocytic leukemia (APL), high rate complete remission as a single agent
107
Arsenic trioxide toxicity *
Atrial or ventricular arrhythmias - lengthening of QT interval on ECG (40% patients)
108
What is the target of arsenic troxide (ATO)?
Relapsed acute promyelocytic leukemia (APL), complete responses in >85% patients

CMBM exam 5 (19 decks)

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