Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm III Exam 1 > Cancer Chemotherapy > Flashcards

Cancer Chemotherapy Flashcards

1
Q

Most common types of cancer?

A

Breast, prostate, lung, colon, melanoma, lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Most common lung cancer deaths?

A

Lung, colon, pancreas, breast, prostate, liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is cancer?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Causes of cancer?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Most DNA mutations are harmless and cause what?

A

Immediate cell death and no harm to pts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

Tumor suppressor genes or oncogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

Filler sequences or genes not related to growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Mutations in tumor suppressor genes remove what?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Solid tumors affect what?

A

Organs and other solid tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are solid tumors are specified by what?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Hematologic malignancies affect what?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is a primary tumor?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Metastasis could be as individual cells or what?

A

New tumor sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Stages used to classify solid tumors?

A

I-IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Stages used to classify hematologic malignancies?

A

I-IV or something else, unique staging methods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Localized therapies for cancer?

A

Surgery, radiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Systemic therapies for cancer?

A

Chemotherapy: traditional, monoclonal antibodies, targeting agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Immunomodulation therapy for cancer?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Surgery goals are dependent upon what?

A

Size, location, type of tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Can surgery be used for hematologic cancers?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Is surgery usually used along with other therapy or alone?

A

With other therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Is radiation usually used along with other therapy or alone?

A

May be used alone or with surgery and/or chemo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What does radiation involve?

A

Exposing the patient to ionizing radiation using high energy photon beams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

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

A

Higher amounts, longer duration, and repeated doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Typical sources of radiation therapy?

A

External beam using cobalt or cesium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What does chemo involve?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How is chemo administered?

A

Typically IV or PO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

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

A

Significant side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Do cancer cells follow the cell cycle like normal cells?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Traditional chemotherapy typically targets which mechanics of cell division?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Examples of traditional chemo?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are newer chemo drugs based on?

A

Identifying mutated proto-oncogenes and tumor suppressor genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Targeted chemo drug classes?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is neoadjuvant chemo?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is adjuvant chemo?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Is chemo dose dependent?

A

Typically, yes
(higher doses kill more cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

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

A

Side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

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

A

Dose limiting toxicities of chemo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

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

A

Desired, but not always possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What does the term “cure” refer to?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What does the term “control” refer to?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What does the term “palliation” refer to?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

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

A

Unable to detect presence of cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

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

A

Reduction of tumor burden but cancer still present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What does the term “stable response” refer to?

A

Tumor still present but has not grown or shrunk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

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

A

Cancer continues to grow despite tx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

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

A

Refractory or resistant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Other reasons chemo would have lack of effect?

A

Drug interactions, food interactions, poor adherence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Salvage treatment option if primary tx is unsuccessful?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Other treatment options if primary tx is unsuccessful?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Older chemo agents use various mechanisms to block what?

A

Cell division w/ limited discrimination between cancer and normal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

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

A

Significant side effects (some are serious but rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What groups of DNA do alkylating agents target?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Are alkylating agents cell cycle specific?

A

NO, cell cycle non-specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Examples of alkylating agents?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Members of the alkylating agents vary by what?

A

Structure and family, but have same general MOA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

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

A

Breast, leukemia, lymphoma, myeloma, etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

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

A

Myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

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

A

Lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Examples of platinum analogs?

A

Cisplatin, Carboplatin, Oxaliplatin “-platin”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Oxaliplatin (platinum analog) is used for what cancers?

A

Colorectal, esophageal, pancreatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Adverse effects of Cisplatin (platinum analog)?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Adverse effects of Carboplatin (platinum analog)?

A

Avoids major toxicities of cisplatin but causes myelosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Adverse effects of Oxaliplatin (platinum analog)?

A

Neurotoxicity (peripheral neuropathy), myelosuppression, diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Many early chemo drugs were of which class?

A

Antimetabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Examples of antimetabolites?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

MOA of Methotrexate (antimetabolite)?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

MOA of Cytarabine (antimetabolite)?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

MOA of 6-MP (antimetabolite)?

A

Inhibits multiple enzymes that synthesize purine nucleotides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Methotrexate (antimetabolite) is used for which cancers?

A

Leukemia, lymphoma, breast, RA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Pemetrexed (antimetabolite) is used for which cancer?

A

Lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Capecitabine (antimetabolite) is used for which cancer?

A

Breast

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?

A

Taxanes

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?

A

Prostate

142
Q

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

A

Breast

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?

A

No

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?

A

Leukemia

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?

A

Lung

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?

A

Breast

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?

A

Thyroid

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?

A

CYP450

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

A

decrease

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?

A

harder

262
Q

What are secondary malignancies most commonly associated with?

A

Alkylating agents and etoposide

Pharm III Exam 1 (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions