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Pharm III Exam 1 > Cancer Chemotherapy > Flashcards

Cancer Chemotherapy Flashcards

1
Q

Most common types of cancer?

A

Breast, prostate, lung, colon, melanoma, lymphoma

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2
Q

Most common lung cancer deaths?

A

Lung, colon, pancreas, breast, prostate, liver

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3
Q

What is cancer?

A

Disease caused by accumulated mutations (nucleotide substitutions that change amino acid sequence and subsequent protein structure/function)

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4
Q

Progression from mutation to cancer?

A

Nucleotide mutation/substitution –> changes nucleotide sequence –> amino acids sequence changes –> protein structure & function could change –> altered cell growth –> cancer may develop

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5
Q

Mutations in cancer cells give them growth advantages over normal cells and enable cancer cells to do what?

A

Use body resources better than normal cells to grow, form tumors, and invade other tissues

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6
Q

Causes of cancer?

A

DNA susceptible to change (mutation, evolution), exposure to chemicals/radiation promotes mutations

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7
Q

Most DNA mutations are harmless and cause what?

A

Immediate cell death and no harm to pts

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8
Q

Mutations that occur in which parts of DNA can lead to altered cell growth/cause cancer?

A

Tumor suppressor genes or oncogenes

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9
Q

What are proto-oncogenes?

A

Sections of DNA that encode for genes used to make specific proteins vital to promote cell growth (kinases, cell surface R’s, regulators of apoptosis)

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10
Q

Mutations of proto-oncogenes cause what?

A

Oncogenes that overstimulate cells to grow/can lead to development of highly abnormal cell growth and development of cancer

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11
Q

Mutations in which parts of DNA do not lead to cancer?

A

Filler sequences or genes not related to growth

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12
Q

What are tumor suppressor genes?

A

Special genes in DNA for proteins which regulate cell growth (serve as mechanism to prevent over stimulating cell growth)

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13
Q

Mutations in tumor suppressor genes remove what?

A

Regulation of cell growth and may lead to excessive cell growth/development of cancer

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14
Q

Difference between mutation of proto-oncogenes and tumor suppressor genes?

A

Proto-ocogenes: overstimulation of cells to grow
Tumor suppressor genes: No limits/regulation of cell growth

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15
Q

Solid tumors affect what?

A

Organs and other solid tissues

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16
Q

What are solid tumors are specified by what?

A

Origin of cell type: squamous cell carcinoma, adenocarcinoma, sarcoma, etc.

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17
Q

Hematologic malignancies affect what?

A

Blood cells (leukemia, lymphoma, hodgkin disease, myeloma)

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18
Q

What is a primary tumor?

A

Original mass of cancer cells of a solid tumor in a body organ

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19
Q

Metastasis could be as individual cells or what?

A

New tumor sites

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20
Q

Stages used to classify solid tumors?

A

I-IV

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21
Q

Stages used to classify hematologic malignancies?

A

I-IV or something else, unique staging methods

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22
Q

Localized therapies for cancer?

A

Surgery, radiation

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23
Q

Systemic therapies for cancer?

A

Chemotherapy: traditional, monoclonal antibodies, targeting agents

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24
Q

Immunomodulation therapy for cancer?

A

Stem cell (bone marrow) transplant, immunosuppressive, immunotherapy, or immunostimulatory agents, CAR-T cell therapy

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25
Q

Surgery goals are dependent upon what?

A

Size, location, type of tumor

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26
Q

Can surgery be used for hematologic cancers?

A

No

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27
Q

Is surgery usually used along with other therapy or alone?

A

With other therapy

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28
Q

Is radiation usually used along with other therapy or alone?

A

May be used alone or with surgery and/or chemo

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29
Q

What does radiation involve?

A

Exposing the patient to ionizing radiation using high energy photon beams

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30
Q

Radiation is similar to energy used in x-rays, but with what?

A

Higher amounts, longer duration, and repeated doses

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31
Q

Typical sources of radiation therapy?

A

External beam using cobalt or cesium

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32
Q

Radioactive energy effects on the body?

A

Electrically charged particles destroy cancer cells and stop them from growing, but may also cause damage to neighboring tissues

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33
Q

What does chemo involve?

A

Use of drugs with various mechanisms of action that disrupt cancer cell function

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34
Q

How is chemo administered?

A

Typically IV or PO

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35
Q

Exposing chemo drugs to both cancerous and normal cells results in what?

A

Significant side effects

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36
Q

Do cancer cells follow the cell cycle like normal cells?

A

Yes, interruption of this cycle can slow/stop tumor growth

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37
Q

Based on knowing that cells need certain molecules to grow, scientists synthesized what to block growth pathways of cancer cells?

A

false analogs (aka antagonists) of vitamins like folic acid

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38
Q

Traditional chemotherapy typically targets which mechanics of cell division?

A

DNA, RNA, DNA polymerase, topoisomerases, spindle fiber formation, etc.

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39
Q

Examples of traditional chemo?

A

Cyclophosphamide, Vincristine, Doxorubicin, Etoposide, Cisplatin, Methotrexate, Paclitaxel, Fluorouracil, etc.

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40
Q

What do newer chemo drugs target?

A

Specific proteins (enzymes, receptors, ligands) required for various cell functions such as growth or apoptosis but are mutated in some way

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41
Q

What are newer chemo drugs based on?

A

Identifying mutated proto-oncogenes and tumor suppressor genes

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42
Q

Targeted chemo drug classes?

A

Tyrosine kinase inhibitors (TKIs), Conjugated monoclonal antibodies, Monoclonal antibodies, Immune checkpoint inhibitors

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43
Q

Mechanism of action method for chemo?

A

Various cancer susceptible to drugs w/ differing MOAs –> giving combos of drugs takes advantage of multiple MOAs to kill cancer cells in different ways

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44
Q

What are the principles of identifying drug combos with chemo?

A

-Efficacy (each drug in a regimen needs anticancer activity when used alone)
-Toxicity (select drugs to minimize overlap of toxicities)
-Optimum scheduling (each drug given in convenient intervals to maximize activity)
-MOA (differing MOAs help overwhelm cells ability to develop resistance)

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45
Q

Timing (relative to local tx) and intent importance in chemo?

A

Local therapy (surgery, radiation) used as primary tx
–> neoadjuvant vs adjuvant chemo

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46
Q

What is neoadjuvant chemo?

A

used before local therapy to reduce tumor/improve local tx success

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47
Q

What is adjuvant chemo?

A

used after to improve long term effect/eliminate remaining undetected cancer cells

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48
Q

Is chemo dose dependent?

A

Typically, yes
(higher doses kill more cells)

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49
Q

Higher doses of chemo kill more cells, yet cause more what?

A

Side effects

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50
Q

What helps determine the “safe doses” of meds for chemo in regards to side effects?

A

Dose limiting toxicities of chemo

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51
Q

What is log cell kill kinetics?

A

A given treatment will kill a constant fraction of cells & subsequent doses reduce cancer burden proportionally over time
*explains why chemo is given as repeated doses over time & not just one dose

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52
Q

What is dose density?

A

Amount of drug/unit of time

–>giving repeated doses of multiple chemo agents over period of time aka chemo cycles (give same drgs once q1-4wks)

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53
Q

Regular exposure to chemo (dose density) provides what?

A

A wave-like approach to killing cancer cells over time
*percentage killed each time pt gets dose of chemo aka log cell kinetics
*time between doses limits side effects/allows body to recover before next dose

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54
Q

Maintaining dose density (avoiding pauses and delays or dose redcutions) is what?

A

Desired, but not always possible

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55
Q

What does the term “cure” refer to?

A

A sustained/prolonged cancer free period (usually 5 years)

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56
Q

What does the term “control” refer to?

A

Reduce cancer burden, prevent extension of cancer, extend survival (cure unlikely)

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57
Q

What does the term “palliation” refer to?

A

Reduce sx, improve quality of life, prolong survival (cure not likely)

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58
Q

What does the term “Remission/complete response (CR)” refer to?

A

Unable to detect presence of cancer

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59
Q

What does the term “partial response (PR)” refer to?

A

Reduction of tumor burden but cancer still present

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60
Q

What does the term “stable response” refer to?

A

Tumor still present but has not grown or shrunk

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61
Q

What does the term “treatment failure/progressive disease (PD)” refer to?

A

Cancer continues to grow despite tx

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62
Q

Goal of cancer as chronic disease?

A

Improve/maintain quality of life and extend survival with drugs to control cancer but nor necessarily cure it

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63
Q

Cancer as chronic disease tx avoids what? What does this lead to?

A

Need to provide overly aggressive/toxic drugs, leads to larger population of patients living w/ cancer w/ different needs

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64
Q

Why is cancer as chronic disease tx not used in all types of CA?

A

As cure is still possible in many situations

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65
Q

How to determine response cancer tx?

A

PE, Radiographs (XR, CT, MRI, PET), Tumor markers (measure conc. of proteins in blood indicating presence of CA/response to tx), Bx/blood tests for presence of cancer cells

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66
Q

What terms are used to describe cancers that have not responded to tx?

A

Refractory or resistant

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67
Q

What can more mutations within cancer cells (chemo resistance) result in?

A

Blocking chemo actions, blocking uptake of chemo into cells, facilitation of excessive transport of drugs back out of cells

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68
Q

Other reasons chemo would have lack of effect?

A

Drug interactions, food interactions, poor adherence

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69
Q

How can drug interactions lead to lack of effect of chemo?

A

(between chemo and non-chemo drugs) can increase metabolism /decrease chemo conc. in patients body

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70
Q

Reasons for food interactions leading to lack of effect of chemo?

A

Specific directions may not be communicated (take w/ or w/o food)

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71
Q

Reasons for poor adherence leading to lack of effect of chemo?

A

Missed clinic appts, missing refills on rx, don’t take meds as prescribed

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72
Q

Salvage treatment option if primary tx is unsuccessful?

A

Using combos of other chemo drugs (2nd line, 3rd line, 4th line)

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73
Q

Stem cell transplant (bone marrow) treatment option if primary tx is unsuccessful?

A

Autologous SCT: high dose chemo followed by re-infusion of pt’s stem cells
Allogenic SCT: chemo + immune modulation + infusion of donor stem cells

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74
Q

Other treatment options if primary tx is unsuccessful?

A

CAR-T cell therapy or investigational therapies (clinical trials)

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75
Q

Older chemo agents use various mechanisms to block what?

A

Cell division w/ limited discrimination between cancer and normal cells

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76
Q

Newer chemo agents target specific functions of cancer cells yet still have what?

A

Significant side effects (some are serious but rare)

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77
Q

What functions can be targets of chemo?

A

DNA/RNA components, Topoisomerases, Mechanics of division (spindle fibers), Enzymes required for making nucleotides (thymide synthase, dihydrofolate reductase), DNA polymerase, Ribonucleotide reductase, Tyrosine kinases, GF receptors

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78
Q

MOA of alkylating agents?

A

Group of molecules that transfer alkyl group to other molecules and disrupts cancer DNA structure by altering molecular interactions/prevents use of DNA as blueprint for cell division

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79
Q

What groups of DNA do alkylating agents target?

A

sulfydryl, amino, hydroxyl, carboxyl, phosphate groups of DNA

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80
Q

Are alkylating agents cell cycle specific?

A

NO, cell cycle non-specific

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81
Q

Examples of alkylating agents?

A

Carmustine, Lomustine, Mechlorethamine, Melphalan, Thiotepa, Procarbazine, Chlorambucil, Cyclophosphamide, Bendamustine, Temozolomide, Dacarbazine

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82
Q

Members of the alkylating agents vary by what?

A

Structure and family, but have same general MOA

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83
Q

Cyclophosphamide (alkylating agent) is used in combo regimens for which cancers?

A

Breast, leukemia, lymphoma, myeloma, etc.

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84
Q

Melphalan (alkylating agent) is used in combo regimens for which cancer?

A

Myeloma

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85
Q

Procarbazine (alkylating agent) is used in combo regimens for which cancer?

A

Lymphoma

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86
Q

Common adverse effects of alkylating agents?

A

Myelosuppression, Mucositis, Sterility (usually temporary but can be prolonged), N/V, tissue damage following extravasation, risk of secondary malignancy

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87
Q

Examples of platinum analogs?

A

Cisplatin, Carboplatin, Oxaliplatin “-platin”

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88
Q

MOA of platinum analogs?

A

Similar to alkylating agents by binding DNA/forming intra- and inter- crosslinks, also bind to cytoplasmic and nuclear proteins required for cell function

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89
Q

Cisplatin and Carboplatin (platinum analogs) are used for which cancers?

A

Lung, esophagus, testicular, ovary, head & neck, bladder

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90
Q

Oxaliplatin (platinum analog) is used for what cancers?

A

Colorectal, esophageal, pancreatic

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91
Q

Adverse effects of Cisplatin (platinum analog)?

A

Renal toxicity (inc. serum Cr, electrolyte wasting: K, Mg), anemia, N/V, ototoxicity

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92
Q

Adverse effects of Carboplatin (platinum analog)?

A

Avoids major toxicities of cisplatin but causes myelosuppression

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93
Q

Adverse effects of Oxaliplatin (platinum analog)?

A

Neurotoxicity (peripheral neuropathy), myelosuppression, diarrhea

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94
Q

What are false analogs (antimetabolites)?

A

Molecules from nature or lab that substitute for actual components of metabolic processes based on similar (but slightly different) structure

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95
Q

General MOA of false analogs (antimetabolites)?

A

Involve themselves like the actual molecule and inhibit normal cell processes that produce component of DNA (sometimes based on structure of vitamins required for enzymatic activity)

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96
Q

Many early chemo drugs were of which class?

A

Antimetabolites

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97
Q

Examples of antimetabolites?

A

Methotrexate, Capecitabine, 5-Fluorouracil, Cytarabine, Gemcitabine, Fludarabine, 6-Mercaptupurine

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98
Q

MOA of Methotrexate (antimetabolite)?

A

Inhibits DHFR (converts one form of folic acid to another, blocks purine synthesis), also inhibits TS

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99
Q

MOA of Capecitabine and 5-FU (antimetabolite)?

A

Inhibits TS, blocks incorporation of FUTP into RNA and dFUTP into DNA (blocking formation of RNA and DNA)

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100
Q

MOA of Cytarabine (antimetabolite)?

A

Mimics cytidine and inhibits DNA polymerase and DNA repair, prevents DNA chain elongation

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101
Q

MOA of Gemcitabine (antimetabolite)?

A

Inhibits ribonucleotide reductase, preventing production of deoxytriphosphates for DNA synthesis, inhibits DNA polymerase blocking DNA synthesis and repair

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102
Q

MOA of Fludarabine (antimetabolite)?

A

Inhibits DNA polymerase that blocks DNA synthesis and repair, inhibits ribonucleotide reductase preventing production of deoxytriphosphates for DNA synthesis

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103
Q

MOA of 6-MP (antimetabolite)?

A

Inhibits multiple enzymes that synthesize purine nucleotides

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104
Q

Methotrexate (antimetabolite) is used for which cancers?

A

Leukemia, lymphoma, breast, RA

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105
Q

Pemetrexed (antimetabolite) is used for which cancer?

A

Lung

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106
Q

Capecitabine (antimetabolite) is used for which cancer?

107
Q

5-FU (antimetabolite) is used for which cancers?

A

Colorectal, esophageal, breast, etc.

108
Q

Cytarabine (antimetabolite) is used for which cancers?

A

Leukemia, lymphoma

109
Q

Gemcitabine (antimetabolite) is used for which cancers?

A

Pancreas, bladder, breast, lung, ovarian

110
Q

Which special antimetabolite has no anticancer action?

A

Leucovorin

111
Q

What is Leucovorin?

A

Reduced form of folic acid that mimics action of engogenous tetrahydrofolate

112
Q

What is Leucovorin used for?

A

-Decreases methotrexate toxicity by rescuing normal cells (bypasses inhibition of dihydrofolate reductase/DHFR by methotrexate)
-Increases 5-FU activity against colon CA (enhances binding of 5-FU to thymidylate synthase/TS)

113
Q

Adverse effect of Methotrexate (antimetabolite)?

A

Mucositis, diarrhea, myelosuppression

114
Q

Adverse effect of Capecitabine (antimetabolite)?

A

Diarrhea, palmar-plantar-erythrodyesthesia (PPE), myelosuppression, N/V

115
Q

How to tx PPE from Capecitabine, Pemetrexed (antimetabolite)?

A

Dexamethasone

116
Q

Adverse effect of 5-FU (antimetabolite)?

A

Mucositis, diarrhea, myelosuppression

117
Q

Adverse effect of Cytarabine (antimetabolite)?

A

Myelosuppression, pulmonary toxicity*, acral erythema, N/V, cerebellar toxicity, ocular toxicity

118
Q

Adverse effect of Gemcitabine (antimetabolite)?

A

N/V, diarrhea, myelosuppression

119
Q

Adverse effect of Pemetrexed (antimetabolite)?

A

Myelosuppression, rash, mucositis, diarrhea, PPE

120
Q

How to reduce adverse effects of Pemetrexed?

A

Vitamin B12 & folic acid supplementation

121
Q

Which chemo agents are derived from natural products?

A

Alkaloids (original molecules extracted from plants), Antitumor abx (derived from micro-organisms like bacteria/fungi)

122
Q

Which family of alkaloids are derived from periwinkle plants?

A

Vinca alkaloids

123
Q

Which family of alkaloids are derived from various types of yew trees?

124
Q

Which family of alkaloids are derived from mayapple roots?

A

Epipodophyllotoxins

125
Q

Which family of alkaloids are derived from the camptotheca acuminata tree?

A

Camptothecins

126
Q

Examples of vinca alkaloids?

A

Vincristine, Vinblastine, Vinorelbine

127
Q

Vinca alkaloids MOA?

A

Inhibit tubulin polymerization required for microtubule assembly and prevent microtubule formation —> blocks cell division during metaphase —> cell death

128
Q

Vincristine (vinca alkaloid) is used for what kinds of cancer?

A

Leukemia, lymphoma, neuroblastoma, Wilm’s tumor, rhabdomyosarcoma

129
Q

Vinblastine (vinca alkaloid) is used for what kinds of cancer?

A

Leukemia, lymphoma, Kaposi’s sarcoma, germ cell cancer

130
Q

Vinorelbine (vinca alkaloid) is used for what kinds of cancer?

A

Lung, breast, ovarian

131
Q

Adverse effects of vinca alkaloids?

A

Alopecia, neurotoxicity (peripheral neuropathy), constipation, myelosuppression, potent vesicant action upon extravasion

132
Q

What is extravasion?

A

Tissue damage from leakage of chemo outside of a vein during administration d/t poor needle placement *can be serious injury

133
Q

What kinds of chemo can cause extravasion?

A

Vinca alkaloids, Anthracyclines

134
Q

S/Sx of extravasion?

A

Pain, redness, burning, pallor, no blood return, edema, decreased IV flow or flush

135
Q

Examples of taxane alkaloids?

A

Paclitaxel, Docetaxel, Cabazitaxel, Ixabepilone (not really a taxane but same MOA)

136
Q

Taxane alkaloid MOA?

A

Promote microtubule formation, preventing spindle fibers from retracting –> blocks completion of cell division and leads to cell death

137
Q

Paclitaxel (taxane alkaloid) is used for what kinds of cancer?

A

Ovarian, Lung, Prostate, Breast, Head & neck, Esophagus, Bladder

138
Q

Protein-bound paclitaxel (taxane alkaloid) is used for what kinds of cancer?

A

Breast, lung, pancreatic (sometimes called albumin bound paclitaxel)

139
Q

What is an advantage of protein bound paclitaxel?

A

Enhances delivery/reduces some toxicity

140
Q

Docetaxel (taxane alkaloid) is used for what kinds of cancer?

A

Breast, Lung, Head & neck, Gastric, Ovarian, Bladder

141
Q

Cabazitaxel (taxane alkaloid) is used for what kind of cancer?

142
Q

Ixabepilone (taxane alkaloid) is used for what kind of cancer?

143
Q

Adverse effects of taxane alkaloids?

A

Myelosuppression, hypersensitivity rxn, peripheral neuropathy, fluid retention (docetaxel)

144
Q

Is nanoparticle albumin-bound paclitaxel (nab-paclitaxel) a substitute for original paclitaxel?

145
Q

nanoparticle albumin-bound paclitaxel (nab-paclitaxel) is only approved for treatment of which cancers?

A

Breast, non-small cell lung, pancreatic

146
Q

How does nanoparticle albumin-bound paclitaxel (nab-paclitaxel) have fewer side effects and better delivery?

A

Avoids use of cremophor found in original paclitaxel which decreases infusion rxns, nano-particle size enhances the delivery to tumor sites, longer half-life, albumin shell escapes recognition by healthy cells

147
Q

Examples of Epipodophyllotoxins (alkaloids)?

A

Etoposide, Teniposide

148
Q

MOA of Epipodophyllotoxins (alkaloids)?

A

Inhibit DNA topoisomerase II –> prevents proper unwinding of DNA, resulting in blockade of DNA synthesis and cell division

149
Q

Etoposide is used for which cancers?

A

Lung, Germ cell, lymphoma, gastric

150
Q

Teniposide is used for which cancer?

A

Pediatric leukemia

151
Q

Adverse effects of Epipodophyllotoxins (alkaloids)?

A

Myelosuppression, alopecia, hypotension (if infused too quickly)

152
Q

How are antitumor abx used for cancer?

A

Compounds produced and used by organisms to compete w/ other organisms for resources, esentially natural cellular toxins, serve as self defense mechanisms that can be chemically isolated/made into anti-cancer agents

153
Q

Examples of antitumor abx?

A

Anthracyclines/Anthracenedione, Doxorubicin, Daunorubicin, Epirubicin, Idarubicin, Mitoxantrone, Mitomycin, Bleomycin

154
Q

MOA of anthracyclines?

A

Multiple: inhibit topoisomerase 2, bind to DNA and intercalate DNA strands, generate to free radicals, bind to cell membranes/alter fluid and ion transport

155
Q

Process of DNA intercalation by anthracyclines?

A

Drug binds to areas on both strands, preventing DNA from being replicated

156
Q

Process of free radical formation by anthracyclines?

A

Free radicals are very damaging to cells by binding to metabolic products, altering structures, disrupting cellular function

157
Q

Doxorubicin (anthracycline) is used for what types of cancer?

A

Breast, Myeloma, Leukemia, Lymphoma

158
Q

Daunorubicin & Idarubicin (anthracyclines) are used for what type of cancer?

159
Q

Epirubicin (anthracycline) is used for which types of cancer?

A

Breast, gastroesophageal

160
Q

Mitoxantrone (anthracycline) is used for which types of cancer?

A

Leukemia, lymphoma, prostate, MS

160
Q

Adverse effects of anthracyclines?

A

Myelosuppression, alopecia, N/V, Mucositis, vesicant if extravasated, cardiotoxicity*

161
Q

Mitoxantrone (anthracycline) causes urine to turn what color?

A

Blue/green

162
Q

Doxo/Dauno/Ida/Epirubicin (anthracycline) causes urine to turn what color?

A

Red/orange

163
Q

Characteristics of acute cardiotoxicity from anthracyclines?

A

W/in 24-72 hrs of administration, arrhythmias, pericarditis, myocarditis, usually subclinical

164
Q

Characteristics of chronic cardiotoxicity from anthracyclines?

A

Dose dependent, delayed by years, results in cardiomyopathy/associated heart failure

165
Q

Cardiotoxicity from anthracyclines can occur at any dose, but risk increases with what?

A

Cumulative dosing
-1-2% risk for doxorubicin doses <300, 6-20% for doxorubicin doses ~500

166
Q

Risk of cardiotoxicity from anthracycline can be mitigated by what?

A

Limiting lifetime doses

167
Q

Use of which anthracycline reduces free radical formation in cardiac tissue yet may reduce therapeutic effect of doxorubicin?

A

Dexrazoxane

168
Q

How can doxorubicin/daunorubicin be formulated to reduce detection/destruction by the immune system?

A

Liposomes (liposomal anthracyclines)

169
Q

How are liposomal anthracyclines an advantage for avoiding cardiotoxicity, N/V, and myelosuppression?

A

Larger size reduces exposure to tightly joined tissue of myocardium/GI tract

170
Q

How can liposomal anthracyclines allow for higher os similar efficacy for tumor cells?

A

Tumors have less tightly joined cells allowing for increased exposure to liposomal chemo

171
Q

Examples of liposomal chemo anthracyclines?

A

Doxil (liposomal doxorubicin), DaunoXome (liposomal daunorubicin)

172
Q

Bleomycin MOA?

A

Binds DNA & forms free radicals thqat destroy DNA and prevent DNA replicatin

173
Q

Bleomycin is used for what types of cancer?

A

Lymphoma, germ cell tumors, head & neck, squamous cell carcinomas

174
Q

Major concern with Bleomycin?

A

Pulmonary toxicity (pneumonitis, cough, dyspnea)

175
Q

What medication is also used as a sclerosing agent/tx for pleural effusions?

A

Bleomycin (cancers within or proximate to the lung more likely to cause pleural effusion)

176
Q

RF for pulmonary toxicity with bleomycin?

A

Age >70, cumulative doses >400u, underlying pulm disease, prior mediastinal radiation, supplemental o2

177
Q

What do tyrosine kinases do?

A

families of proteins that use ATP to phosphorylate other proteins/control their function (usually enzymatic R’s on the surface of cells)

178
Q

What happens when tyrosine kinases are mutated in cancer cells?

A

Often become overactive and lead to enhanced tumor growth (examples of potential proto-oncogenes and tumor suppressor genes)

179
Q

Examples of TK’s in humans?

A

C-Kit, Epidermal GF Receptor, BCR-ABL (philadelphia chromosome), JAK, Platalet derived GF receptor, human epidermal R

180
Q

TKIs MOA?

A

Target, bind to, and block activity of various TK’s like an antagonist, resulting in inhibition of specific pathways and promotes cancer cell death through apoptosis
*also starting to be used for RA, organ transplant, Crohns, UC

181
Q

Examples of TKIs?

A

Axitinib, Bosutinib, Gefitinib “end in -inib”

182
Q

Differences between TKIs?

A

Target different TKs present in different kinds of cancers, differ in binding affinity to their targets (make some more potent/bind with less restriction –> reduces chances for resistance, inc types of TKs they bind to)

183
Q

How does resistance to TKIs develop?

A

When more mutations occur in the amino acid sequence of the TK that is targeted by the TKI after the drug has been started, which prevent it from binding/make the drug ineffective

184
Q

Axitinib (TKI) is used for what type of cancer?

A

Renal cell carcinoma

185
Q

Imatinib, dasatinib, nilotinib, bosutinib, ponatinib (TKIs) are used for what type of cancer?

A

Chronic myelogenous leukemia, Ph+ acute lymphoblastic leukemia

186
Q

Crozptinib and Gefitinib (TKIs) are used for what type of cancer?

187
Q

Erlotinib (TKI) is used for what type of cancer?

A

Lung, pancreatic

188
Q

Ibrutinib, Acalabrutinib, Zanubrutinib (TKIs) are used for what type of cancer?

A

Chronic lymphocytic leukemia, lymphoma

189
Q

Lapatinib (TKI) is used for what type of cancer?

190
Q

Levatinib (TKI) is used for what type of cancer?

A

Hepatocellular carcinoma, renal cell, thyroid

191
Q

Pazopanib (TKI) is used for what type of cancer?

A

Renal cell carcinoma, sarcoma

192
Q

Regorafenib (TKI) is used for what type of cancer?

A

Colorectal, gastrointestinal stromal tumor, hepatocellular carcinoma

193
Q

Sorafenib and Sunitinib (TKIs) are used for what type of cancer?

A

Renal cell

194
Q

Vanderanib (TKI) is used for what type of cancer?

195
Q

Adverse effects of TKIs?

A

Rash, myelosuppression, fatigue, fluid retention, diarrhea, myalgia, congestive HF, QT prolongation, Afib, bleeding, HTN, hepatotoxicity

196
Q

What are TKIs metabolized by that cause them to have many drug interactions?

197
Q

Enzyme inhibitors (azole antifungals) can _____ metabolism and _____ side effects of TKIs

A

decrease metabolism, increase SE

198
Q

Enzyme inducers (phenytoin) can _____ metabolism and _____ effectiveness of TKIs

A

increase metabolism, decrease effectiveness

199
Q

Reduced bioavailability w/ concomitantuse of stomach acid reducers (H2A, PPIs) can _____ effectiveness of some TKIs

200
Q

Immunomodulators MOA?

A

Unclear, may alter tumor necrosis factor TNF levels/increase activity of NK cells, IL-2, interferons/promote apoptosis

201
Q

Immunomodulators are mostly used in combination with ______ to treat what?

A

Dexamethasone, Multiple myeloma

202
Q

Examples of immunomodulators?

A

Thalidomide, Lenalidomide (preferred based on efficacy), Pomalidomide

203
Q

Adverse effects of immunomodulators?

A

Peripheral neuropathy, thromboembolism, fatigue, rash, myelosuppression, dizziness/drowsiness, birth defects (REMS program w/ pt, prescriber, pharmacist)

204
Q

Proteasome inhibitors MOA?

A

Inhibit complexes of proteins that would otherwise break down unneeded or damaged proteins –> promote activation of signaling pathways that trigger apoptosis

205
Q

Proteasome inhibitors are used for what?

A

Multiple myeloma

206
Q

Examples of proteasome inhibitors?

A

Bortezomib (preferred based on efficacy), Carfilzomib, Ixazomib

207
Q

Adverse effects of proteasome inhibitors?

A

Peripheral neuropathy, neuralgia, rash, N/V/D, myelosuppression, heart failure, activation of Herpes Zoster/Herpes Simplex (requires antiviral prophylaxis), pulmonary toxicity

208
Q

Monoclonal antibodies MOA?

A

Specifically designed antibodies made using biotechnology to target specific proteins in cancer cells/block their standard function (usually bind to various sites on receptors: EGFR, HER2, CD antigens)

209
Q

Examples of monoclonal antibodies?

A

Trastuzumab, Cetuximab, Pertuzumab, Panitumumab, Bevacizumab, Alemtuzumab, Rituximab, etc.

210
Q

How are monoclonal antibodies derived in order to reduce risk of adverse effects?

A

Derived from animals and then humanized

211
Q

Names of monoclonal antibodies are made of what 4 parts?

A

Prefix (company specific), target substem (tu-tumor, ci-circulatory), source substem (zu-humanized, xi-humanized/chimeric, mu-mouse), suffix (mab)

212
Q

Possible ways monoclonal antibodies are thought to kill tumor cells?

A

Block R’s required to activate cell functions, bind to free protein ligands looking to bind to R’s, bind to receptors and trigger apoptosis, bind to R’s and trigger antibody-dependent cellular toxicity (ADCC)

213
Q

What is Rituximab used for?

A

CD20+ lymphoma

214
Q

What is Trastuzumab used for?

A

Her2/neu overexpressing breast cancer

215
Q

What is Cetuximab used for?

A

Colorectal CA, head and neck CA, lung CA

216
Q

What is Panitumumab used for?

A

Colorectal CA

217
Q

What is Bevacizumab used for?

A

Colorectal, breast, lung, and renal cell cancers

218
Q

Adverse effects of monoclonal antibodies?

A

Infusion rxns (premedicate w/ acetaminophen, diphenhydramine +/- dexamethasone)

219
Q

Drug specific reactions to Bevacizumab?

A

Arterial thromboembolic events, delayed wound healing, gastrointestinal perf

220
Q

Drug specific reactions to Trastuzumab?

A

Heart failure

221
Q

Drug specific reactions to Panitumumab/Cetuximab?

A

Interstitial lung disease, hypomagnesemia

222
Q

What are conjugated monoclonal antibodies?

A

Cytotoxic molecules or radioactive particles attached to monoclonal antibodies serving as delivery vehicles to cancer cells

223
Q

Examples of conjugated monoclonal antibodies?

A

fam-trastuzumab deruxetan, ado-trastuzumab emtansine, gemtuzumab ozogamicin, inotuzumab ozogamicin, ibritumomab tiuxetan

224
Q

What are immune checkpoint inhibitors?

A

Some tumors evade the immune system using surface proteins (programmed death ligand: PD-L1 and PD-L2) that interact with PD-1 R’s and inactivate cancer destroying T-cells
–> Nivolumab and Prmbrolizumab (monoclonal abs) target PD-1 R on T-cells/block interaction w/ PD-L1 and PD-L2 that prevent inactivation of cancer-destroying T-cells allowing for an antitumor response

225
Q

Examples of checkpoint inhibitors?

A

Atezolizumab, Avelumab, Durvalumab, Ipilimumab, Nivolumab, Pembrolizumab

226
Q

Since checkpoint inhibitor agents only work if the cancer cells are positive for target checkpoint protein (ligand), what must be done?

A

Testing on the tumor to be able to determine the presence/level of checkpoint proteins
*helps identify patients that will best respond to the agents/individualize cancer therapy

227
Q

Adverse effects of checkpoint inhibitors?

A

Pneumonitis, hepatitis, colitis, endocrinopathies (thyroid, adrenal, pituitary d/o, diabetes), nephritis, rash, infections, infusion rxns

228
Q

What is asparaginase?

A

Enzyme antineoplastic agent that breaks down asparagine to aspartate

229
Q

Which cells are unable to make asparagine?

A

Lymphocytic leukemia (but normal cells can)

230
Q

Administering asparaginase can break down available asparagine and do what to lymphocytic leukemia cells?

A

Deprive them of the necessary amino acid, leading to cell stress/apoptosis

231
Q

Forms of asparaginase?

A

E. coli asparaginase (Elspar)** MC used, PEG-aspargase (Oncaspar) –> long acting/bound to polyethylene glycol molecule, Erwinia asparaginase (made from Erwina yeast, use in pts with hypersensitivity rxn to E.coli)

232
Q

Asparaginase can be used in combo with other drugs to treat what?

A

Acute lymphoblastic leukemia (ALL)

233
Q

Adverse effects of asparaginase?

A

Hypersensitivity (fever, chills, N/V, rash, urticaria, hypotension, dyspnea), clotting/bleeding d/o, pancreatitis, neurologic toxicity

234
Q

What is CAR T cell immunotherapy (CAR-T)?

A

Adoptive cell therapy that is a complex preparation process performed by a manufacturer

235
Q

CAR-T process?

A

T cells harvested from pt –> genetically engineered using neutralized virus –> infects T cells w/ gene that increases production of chimeric antigen R’s –> engineered T-cells expanded in vitro –> re-infused into pt –> CARs enhance binding of T-cells to CD19 antigens on leukemia/lymphoma cells/kill them

236
Q

CAR-T products available?

A

Yescarta, Kymriah, Breyanzi, Tecartus, Abecma, Carvykti

237
Q

Indications for Yescarta?

A

Adult pts w/ R/R large B-cell lymphoma after 2+ lines of systemic tx

238
Q

Indications fotr Kymriah?

A

Patients up to 25 with R/R B-cell, ALL adults w/ R/R B-cell lymphoma or follicular lymphoma after 2+ lines of tx

239
Q

Indications for Breyanzi?

A

Adult patients w R/R large B-cell lumphoma after 2+ lines of systemic tx

240
Q

Indications for Tecartus?

A

Adults with mantle cell lymphoma or all following disease progression

241
Q

Indications for Abecma and Carvykti?

A

Adults w/ R/R multiple myeloma after 4+ lines of tx

242
Q

How is CART tx given?

A

Single infusion fgenerally after other chemo

243
Q

How to prep for possible infusion rxn with CART?

A

Pre medicate w/ acetaminophen and H1A
**Do not use corticosteroids unless life threatening situation

244
Q

What is likely with CART?

A

Hypogammaglobulinemia and prolonged cytopenias

245
Q

BBW for risk/potentially fatal for CART tx?

A

Cytokine rlease syndrome, neuro toxicity, hemophagic lymphoshistocytosis/macrophage activation syndrome, prolonged and recurrent cytopenia

246
Q

What is cytokine release syndrome w CARTS?

A

Fever, hypotension, hypoxia, arrhythmias, cardiac arrest, cardiac failure, renal insufficiency, etc.

247
Q

How to manage cytokine release syndrome w CARTS?

A

Monitor for at least 7 days as inpatients and at least 4wks after infusion for rxn
If indicated: supportive therapy with tocilizumab +/- corticosteroids
*only give corticosteroids if life threatening (will kill re-engineered cells/negate the tx)

248
Q

What kind of neurotoxicity with CARTS?

A

Encephalopathy, headache, delirium, anxiety, dizziness, tremor, peripheral neuropathy, seizures

249
Q

How to manage neurotoxicity with CARTS?

A

Monitor for at least 4wks after infusion, recommend patients not drive, do hazardous activities, operate machinery for at least 8 wks after infusion

250
Q

Goal of phase I clinical trials for chemo?

A

Assess safety (dose ranges, schedule, efficacy) ~10-20 pts who have not responded to other tx, test in multiple types of CA

251
Q

Goal of phase II clinical trials for chemo?

A

Assess efficacy (safety, dosing) longer trial w/ more pts (20-40), focus on effect in pts w/ specific cancers who have not responded to other tx

252
Q

Goal of phase III clinical trials for chemo?

A

Assess efficacy compared to standard tc (RCT) and safety (larger than phase II) focusing on stages of specific diseases which approval will be sought

253
Q

Genetic factors for selecting treatment?

A

Studies identified specific agents/regimens that are more active in patients w/ specific mutations
*PCR tests at time of dx to identify mutations/target tx

254
Q

Targeted treatment for patients with BRAF V600E mutation?

A

Vemurafenib, Dabrafenib, Encorafenib

255
Q

Targeted treatment for patients with MEK (BRAF V600K) mutation?

A

Trametinib, Cobimetinib, Binimetinib

256
Q

Targeted treatment for patients with IDH1 mutation?

A

Ivosidenib

257
Q

Targeted treatment for patients with IDH2 mutation?

A

Enasidenib

258
Q

Targeted treatment for patients with MEK HER2 mutation?

A

Trastuzumab

259
Q

Targeted treatment for patients with PH mutation?

A

Imatinib, Dasatinib

260
Q

What are the most common secondary cancers?

A

Acute leukemia or lymphoma

261
Q

Are secondary malignancies harder or easier to treat than primary cancers?

262
Q

What are secondary malignancies most commonly associated with?

A

Alkylating agents and etoposide

Pharm III Exam 1 (2 decks)

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