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Pharm III - Exam 3 > Oncology > Flashcards

Oncology Flashcards

1
Q

Describe log cell kill kinetics

A
  1. A given treatment kills a constant fraction of cells
  2. Subsequent doses reduce cancer burden proportionally over time
  3. More cells killed, higher chance for cure
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2
Q

Describe Gompertzian model of tumor cell growth

A

Growth fraction of a tumor is NOT constant
-As tumor gets larger, growth fraction decreases
-This results in lower number of cells susceptible to chemo
(so treat earlier!)

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3
Q

What are the principles of combining chemo drugs?

A
  1. Efficacy: each drug must have some anticancer activity on its own
  2. Toxicity: minimize overlapping toxicities
  3. Optimum scheduling: give each drug in intervals to maximize its activity
  4. MOA: multiple to help overwhelm cells’ ability to develop resistance
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4
Q

Describe first line local primary therapy

A

Used in advanced cancer cases in which systemic treatments would NOT be effective

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5
Q

Describe neoadjuvant chemo

A

Used PRIOR to local therapies to improve their effect by reducing size of the tumor

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6
Q

Describe adjuvant chemo

A

Used AFTER local therapies to improve their long term effect by eliminating any remaining undetected cancer cells

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7
Q

Describe dose density of chemo

A
  • Give repeated doses of multiple agents over a period of time
  • Regular exposure provides a wave-like approach to killing cancer cells over time
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8
Q

Define cure in relation to cancer

A
  • Sustained cancer-free period

- Usually 5 years

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9
Q

Define control of cancer

A
  • Reduce cancer burden
  • Prevent extension of cancer
  • Extend survival
  • Cure unlikely
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10
Q

Define palliation

A
  • Reduce symptoms of disease
  • Improve QOL
  • Prolong survival
  • Cure not likely
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11
Q

Define remission/complete response (CR)

A

Unable to detect presence of cancer

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12
Q

Define partial response

A

Reduction in tumor burden but cancer still present

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13
Q

Define treatment failure/progressive disease

A

Cancer continues to grow despite treatment

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14
Q

How can chemo resistance develop?

A
  • Mutations within cancer cells could block chemo actions/uptake, transport drug back out
  • Drug interactions could decrease exposure to chemo within the body
  • Calculated doses could not match pts individual body characteristics
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15
Q

What are the options if primary cancer treatment is unsuccessful?

A
  • Salvage treatment (use other combos)
  • SCT
  • Investigational therapies
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16
Q

Define autologous SCT

A

High dose chemo followed by re-infusion of pt’s own stem cells

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17
Q

Define allogeneic SCT

A

Chemo and immune modulation plus infusion of DONOR stem cells

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18
Q

What are the cell cycle non-specific chemo agents?

A

CAP’N

  • Cytotoxic abx
  • Alkylating agents
  • Platinum compounds
  • Natural products
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19
Q

MOA alkylating agents

A
  • Disrupts normal DNA structure
  • Prevents use of DNA as blueprint for cell division
  • Cell cycle NON-specific
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20
Q

Examples of alkylating agents

A
  • Melphalan
  • Procarbazine
  • Cyclophosphamide
  • Carmustine
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21
Q

Indications for cyclophosphamide

A

Breast cancer, leukemia, lymphoma, myeloma, etc. etc.

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22
Q

Indications for melphalan

A

Myeloma

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23
Q

Indications for procarbazine

A

Lymphoma

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24
Q

Alkylating agents ADEs

A
  • BM toxicity (myelosuppression)
  • Mucositis
  • Sterility (usually temporary)
  • NV
  • Tissue damage (following extravasation)
  • Risk of secondary malignancies
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25
Q

MOA platinum analogs

A

Unclear

  • Likely act similar to alkylating agents by binding DNA and forming crosslinks
  • Also bind to cytoplasmic and nuclear proteins required for cell function
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26
Q

Examples of platinum analogs

A
  • Cisplatin
  • Carboplatin
  • Oxaliplatin
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27
Q

Indications for cisplatin and carboplatin

A 
BELHOT
Bladder
Esophagus
Lung
Head and neck
Ovary
Testicular
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28
Q

Indications for oxaliplatin

A

PEC
Pancreatic
Esophageal
Colorectal

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29
Q

Cisplatin ADEs

A
  • Renal (increase ser Cr, K/Mg wasting)
  • Anemia
  • NV
  • Ototoxicity
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30
Q

Carboplatin ADEs

A

Avoids the major toxicities a/w cisplatin BUT causes myelosuppresison

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31
Q

Oxaliplatin ADEs

A
  • Neurotoxicity (peripheral neuropathy)
  • Myelosuppression
  • Diarrhea
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32
Q

What are antimetabolites?

A
  • Molecules (natural or artificial) that sub for actual components of metabolic processes
  • Inhibits normal cell processes that produce components of DNA
  • S phase specific
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33
Q

Examples of antimetabolites

A
  • MTX
  • Capecitabine
  • Cytarabine
  • Gemcitabine
  • Fludarabine
  • 5-FU
  • 6-MP
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34
Q

MTX MOA

A
  • Antimetabolite
  • Inhibits DHFR which converts one form of folic acid to another
  • Inhibits TS
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35
Q

Capecitabine MOA

A
  • Antimetabolite
  • Inhibits TS
  • Blocks incorporation of FUTP into RNA and dFUTP into DNA (blocking formation of RNA/DNA)
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36
Q

5-FU MOA

A
  • Antimetabolite
  • Same MOA of capecitabine
  • Inhibits TS
  • Blocks incorporation of FUTP into RNA and dFUTP into DNA (blocking formation of RNA/DNA)
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37
Q

Cytarabine MOA

A
  • Antimetabolite
  • Mimics cytidine
  • Inhibits DNA pol and DNA repair that prevents DNA chain elongation
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38
Q

Gemcitabine MOA

A
  • Antimetabolite
  • Inhibits ribonucleotide reductase
  • Prevents production of deoxytriphosphates for DNA synthesis
  • Inhibits DNA pol which blocks DNA synthesis and repair
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39
Q

Fludarabine MOA

A
  • Antimetabolite

- Same as gemcitabine

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40
Q

6-MP MOA

A
  • Antimetabolite

- Inhibits multiple enzymes that synthesize purine nucleotides

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41
Q

Indications for MTX

A
  • Leukemia
  • Lymphoma
  • Breast cancer
  • RA
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42
Q

Indications for pemetrexed

A

Lung cancer

antimetabolite

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43
Q

Indications for capecitabine

A

Breast cancer

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44
Q

Indications for 5-FU

A

-Breast cancer
-Esophageal
-Colorectal
etc etc

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45
Q

Indications for cytarabine

A

Leukemia and lymphoma

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46
Q

Indications for gemcitabine

A 
Pancreas
Bladder
Breast
Lung
Ovarian cancers
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47
Q

What is leucovorin? What does it do?

A
  • Special antimetabolite: NO anticancer action
  • Reduced form of folic acid
  • Mimics action of tetrahydrofolate
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48
Q

Key uses of leucovorin

A
  1. Reduces MTX toxicity by rescuing normal cells

2. Increases 5-FU activity against colon cancer

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49
Q

MTX ADEs

A
  • Mucositis
  • Diarrhea
  • Myelosuppression
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50
Q

Capecitabine ADEs

A
  • Palmar plantar erythrodysesthesia (hand-foot syndrome)
  • Diarrhea
  • NV
  • Myelosuppression
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51
Q

Which antimetabolites may cause hand-foot syndrome?

A

Capecitabine

Pemetrexed

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52
Q

How is hand-foot syndrome prevented/treated?

A

Dexamethasone

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53
Q

5-FU ADEs

A
  • Mucositis
  • Diarrhea
  • Myelosuppression
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54
Q

Cytarabine ADEs

A
  • Acral erythema
  • Cerebellar toxicity
  • Pulm toxicity
  • NV
  • Myelosuppression
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55
Q

Gemcitabine ADEs

A
  • Diarrhea
  • NV
  • Myelosuppression
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56
Q

Pemetrexed ADEs

A
  • Hand foot syndrome
  • Mucositis
  • Diarrhea
  • Rash
  • Myelosuppression
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57
Q

How are ADEs of pemetrexed reduced?

A

B12 and folic acid supplements

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58
Q

Chemo classes derived from natural products

A
  1. Vinca alkaloids (periwinkle plant)
  2. Taxanes (yew trees)
  3. Epipodophyllotoxins (mayapple root)
  4. Camptothecins (Camptothecin acuminata tree)
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59
Q

Vinca alkaloids MOA

A
  • Inhibit tubulin polymerization required for microtubule assembly
  • Results in blocked cell division and causes cell death
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60
Q

Indications for vincristine

A
  • Leukemia
  • Lymphoma
  • Neuroblastoma
  • Wilm’s tumor
  • Rhabdomyosarcoma
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61
Q

Indications for vinblastine

A
  • Leukemia
  • Lymphoma
  • Kaposi’s sarcoma
  • Germ cell cancer
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62
Q

Indications for vinorelbine

A
  • Lung
  • Breast
  • Ovarian cancer
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63
Q

Vinca alkaloids ADEs

A
  • Alopecia
  • Neuro (peripheral neuropathy)
  • Constipation
  • Myelosuppression
  • Potent vesicant action upon extravasation
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64
Q

Taxanes MOA

A
  • Promote microtubule formation

- Prevent disassembly of microtubules, blocking completion of cell division and leads to cell death

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65
Q

Examples of taxane agents

A
  • Paclitaxel
  • Docetaxel
  • Cabazitaxel
  • Ixabepilone
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66
Q

Indications for paclitaxel

A
  • Ovary
  • Lung
  • Prostate
  • Breast
  • Head and neck
  • Esophageal
  • Bladder
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67
Q

Indications for docetaxel

A
  • Breast
  • Lung
  • Head and neck
  • Gastric
  • Ovary
  • Bladder
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68
Q

Indications for cabazitaxel

A

Prostate cancer

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69
Q

Indications for ixabepilone

A

Breast cancer

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70
Q

Taxanes ADEs

A
  • Myelosuppression
  • Hypersensitivity reactions
  • Peripheral neuropathy
  • Fluid retention (docetaxel)
71
Q

Which taxane causes fluid retention?

A

Docetaxel

72
Q

Epipodophyllotoxins MOA

A
  • Inhibit DNA topoisomerase II

- Prevents proper unwinding of DNA resulting in blockade of DNA synth and cell division

73
Q

Examples of epipodophyllotoxins

A

Etoposide

Teniposide

74
Q

Indications for etoposide

A
  • Lung
  • Germ cell
  • Lymphoma
  • Gastric cancer
75
Q

Indications for teniposide

A

Pediatric leukemia

76
Q

Epipodophyllotoxins ADEs

A

HAM

  • Hypotension (if infused too quickly)
  • Alopecia
  • Myelosuppression
77
Q

What are antitumor antibiotics?

A
  • Derived from bacteria to compete for resources

- Anthracyclines (doxorubicin, daunorubicin, bleomycin, etc.)

78
Q

Anthracyclines MOA

A
  • Inhibit topoisomerase 2
  • Bind to DNA and intercalate strands
  • Generate free radicals
  • Bind to cell membranes and alter fluid/ion transport
79
Q

Indications for doxorubicin

A
  • Breast cancer
  • Myeloma
  • Leukemia
  • Lymphoma
80
Q

Indications for daunorubicin and idarubicin

A

Leukemia

81
Q

Indications for epirubicin

A
  • Breast

- Gastroesopageal

82
Q

Indications for mitoxantrone

A
  • Leukemia
  • Lymphoma
  • Prostate
  • MS
83
Q

Which anthracycline can be used in MS?

A

Mitoxantrone

84
Q

Anthracyclines ADEs

A
  • Mucositis
  • Alopecia
  • Myelosuppression
  • NV
  • Vesicant if extravasated
  • Cardiotoxicity
85
Q

ADE of mitoxantrone

A

Turns urine blue/blue-green

86
Q

ADE of doxo/dauno/ida/epirubicin

A

Turns urine reddish-orange

87
Q

Which anthracyclines turn urine blue or blue-green?

A

Mitoxantrone

88
Q

Which anthracyclines turn urine reddish-orange?

A

Doxorubicin
Idarubicin
Epirubicin
Daunorubicin

89
Q

Describe cardiotoxicity of anthracyclines

A
  • Acute: within 24-72 hrs, usually subclincial, arrhythmias/pericarditis/myocarditis
  • Chronic: dose dependent, delayed by years, results in cardiomyopathy and associated heart failure
90
Q

What dose can cardiotoxicity of anthracyclines occur?

A

Any dose, but risk increases with cumulative dosing

91
Q

What is dexrazoxane used for?

A
  • To mitigate cardiotoxicity of anthracyclines
  • Reduces free radical formation in cardiac tissue
  • May reduce therapeutic effect of doxorubicin though
92
Q

What is a major concern of bleomycin use?

A

Pulmonary toxicity

93
Q

Risk factors for pulm toxicity with bleomycin use?

A
  • Age over 70
  • Cumulative doses over 400 units
  • Underlying pulm disease
  • Prior mediastinal radiation
  • Supplemental oxygen
94
Q

What is bleomycin used for?

A
  • Lymphoma
  • Germ cell
  • Head and neck
  • Squamous cell cancers
  • Sclerosing agent for pleural effusions
95
Q

What are tyrosine kinases?

A
  • Families of proteins that use ATP to phosphorylate other proteins
  • Often over active in cancer cells leading to enhanced tumor growth
96
Q

TKI MOA

A
  • Block tyrosine kinases
  • Results in inhibiting specific regulatory pathways
  • Promotes cancer cell death
97
Q

How can resistance to TKIs develop?

A

Mutations in AA sequence of the specific tyrosine kinase could prevent a TKI from binding the targeted site

98
Q

Which TKIs are indicated for Ph+ CML and ALL?

A
  • Bosutinib
  • Imatinib
  • Nilotinib
  • Dasatinib
  • Ponatinib (off market)
99
Q

Indications for erlotinib

A

Lung and pancreatic cancer

100
Q

Which TKIs are indicated for renal cell cancer?

A

Sorafenib and sunitinib

101
Q

Indications for lapatinib

A

Breast cancer

102
Q

Indications for crizotinib

A

Lung cancer

103
Q

Indications for gefinitib

A

Lung cancer

off market now

104
Q

TKI ADEs

A
  • Rash
  • Myelosuppression
  • Fatigue
  • Fluid retention
  • Diarrhea
  • Myalgia
  • CHF
105
Q

Drug interactions with TKIs

A

CYP450

  • Inhibitors (like azoles) can decrease metabolism
  • Inducers (like phenytoin) can increase metabolism
  • Reduced availability with PPIs and H2 blockers
106
Q

Immunomodulators MOA

A

Unclear

  • May alter TNF levels
  • May increase NK cells, IL2, interferon activity
  • May promote apoptosis
107
Q

What are immunomodulators MC used to treat?

A

Myeloma

usually combined with dexamethasone

108
Q

Examples of immunomodulators

A

Thalidomide
Lenalidomide
Pomalidomide

109
Q

Immunomodulators ADEs

A
  • Peripheral neuropathy
  • Thromboembolism
  • Fatigue
  • Rash
  • Myelosuppression
  • Dizzy/drowsy
110
Q

Proteasome inhibitor MOA

A
  • Inhibit complexes of proteins that would otherwise break down unneeded or damaged proteins
  • Promote activation of apoptosis pathways
111
Q

Indications for proteasome inhibitors

A

Myeloma

112
Q

Examples of proteasome inhibitors

A

Bortezomib

Carfilzomib

113
Q

Proteasome inhibitor ADEs

A
  • Activation of herpes zoster/simplex
  • Pulm toxicity
  • Diarrhea, NV
  • Myelosuppression
  • Neuralgia
  • Peripheral neuropathy
  • Heart failure
114
Q

How to identify monoclonal antibodies

A
  • Prefix: company specific
  • Target: tu is tumor, ci is circulatory system
  • Source: zu is humanized, xi is humanized/chimeric, mu is mouse
  • Suffix: mab
115
Q

How mAb kill tumor cells?

A

Not always clear, could be multiple mechanisms

  • Block receptors
  • Bind free protein ligands looking to bind receptors
  • Bind to receptors and trigger apoptosis or ADCC
116
Q

Indications for rituximab

A

CD20 positive lymphoma

117
Q

Indications for trastuzumab

A

HER2/neu overexpressing breast cancer

118
Q

Indications for cetuximab

A
  • Lung
  • Head and neck
  • Colorectal cancer
119
Q

Indications for panitumumab

A

Colorectal cancer

120
Q

Indications for bevacizumab

A
  • Colorectal
  • Breast
  • Lung
  • Renal cell cancers
121
Q

mAb ADEs

A

Infusion related reactions (give premeds - acetaminophen, diphenhydramine plus or minus dexamethasone)

122
Q

How to avoid infusion reactions with mAbs?

A

Give premeds (acetaminophen, diphenhydramine plus or minus dexamethasone)

123
Q

Bevacizumab ADEs

A
  • GI perforation
  • Arterial thromboembolic events
  • Delayed wound healing
124
Q

Trastuzumab ADEs

A

Heart failure

125
Q

Panitumumab and cetuximab ADEs

A
  • Hypomagnesemia

- Interstitial lung disease

126
Q

What is asparaginase and how does it work?

A
  • Enzyme antineoplastic agent

- Breaks down aspargine to aspartate (deprives tumor cells of necessary AA and leads to apoptosis)

127
Q

MC used form of asparaginase?

A

E coli asparaginase

128
Q

Forms of asparaginase

A
  • E coli asparaginase
  • PEG-aspargase (long acting)
  • Erwinia asparaginase (for pts who have hypersensitivity reaction to E coli form)
129
Q

Indications for asparaginase

A

Part of combo chemo to treat ALL

130
Q

Asparaginase ADEs

A
  • Hypersensitivity
  • Clotting and bleeding d/os
  • Pancreatitis
  • Neuro toxicity
131
Q

Goal of phase I clinical trials

A

Assess safety (10-20 pts)

132
Q

Goal of phase II clinical trials

A

Assess efficacy (20-40 pts)

133
Q

Goal of phase III clinical trials

A

Assess efficacy compared to standard treatment (lots of patients, randomized)

134
Q

Describe ALL

A
  • Children
  • Induction, consolidation, maintenance therapy
  • Combo treatment over 2-3 yrs
  • Requires intrathecal chemo d/t chance for spread to CNS
  • Good chance for cure
135
Q

Quick hits: AML

A
  • Adults
  • Induction and consolidation treatment
  • 7 plus 3 regimen (cytarabine, daunorubicin)
  • Some pts considered for ASCT
136
Q

Quick hits: CML

A
  • Philly chromosome
  • Chronic, accelerated, blast stages
  • Use TKIs to control disease
  • ASCT only known cure
137
Q

Quick hits: CLL

A
  • Elderly
  • Treat when symptomatic
  • Many options and aimed at controlling symptoms, prolonging survival
  • Little chance for cure
138
Q

Quick hits: Hodgkin’s lymphoma

A
  • Reed-Sternberg cells
  • EBV related
  • Classic B symptoms (fever, night sweats, wt loss)
  • Lymphadenopathy
  • Several months of chemo plus or minus XRT
  • ABVD regimen
139
Q

Quick hits: NHL

A
  • B symptoms and lymphadenopathy
  • NO RS cells like HL
  • CHOP or R-CHOP (if CD20 positive)
140
Q

Quick hits: myeloma

A
  • Malignant plasma cells produce abnormal IGs
  • Only stages 2 and 3 receive treatment
  • Requires pain and anemia management
  • Bisphosphonates to control bone lesions
141
Q

Quick hits: breast cancer

A
  • Both men and women
  • Screening is key
  • Treatment based on stage and pre/postmeno status
  • Cure possible in all but stage IV disease
142
Q

Quick hits: prostate cancer

A
  • Elderly men
  • Treatment not always provided
  • Treatment types: hormonal, chemo, brachytherapy, surgical
  • Monitor PSA and androgen levels for response to treatment
143
Q

MC GI cancer?

A

Colorectal

144
Q

Quick hits: colorectal cancer

A
  • MC GI cancer

- Common chemo regimens: FOLXFOX, FOLFIRI

145
Q

FOLFOX and FOLFIRI are common chemo regimens for which cancer?

A

Colorectal

146
Q

Quick hits: ovarian cancer

A
  • Typically slow growing and difficult to detect until later stages
  • Chemo options: paclitaxel with cisplatin/carboplatin, topotecan, altretamine, liposomal doxorubicin
147
Q

Quick hits: testicular cancer

A
  • Younger population 20s-40s

- Combo chemo: BEP (bleomycin, etoposide, cisplatin), ICE (ifosfamide, cisplatin, etoposide)

148
Q

Quick hits: malignant melanoma

A
  • Curable in early stages w/surgery
  • Mets is relatively drug-resistant
  • Chemo aims to prolong survival (dacarbazine, temozolomide, cisplatin, aldesleukin)
149
Q

Quick hits: brain cancer

A
  • Multiple types

- Require chemo to be able to cross BBB (carmustine, lomustine, temozolomide)

150
Q

Which chemos can cross BBB?

A

Carmustine
Lomustine
Temozolomide

151
Q

Quick hits: secondary malignancies

A
  • Caused by previous XRT/chemo
  • MC acute leukemia or lymphoma
  • More difficult to treat
  • MC a/w alkylating agents and etoposide
152
Q

What is the MC type of secondary cancer?

A

Usually acute leukemia or lymphoma

153
Q

What agents are MC a/w development of secondary cancers?

A

Alkylating agents and etoposide

154
Q

Define vesicant

A

Blistering agent - severe skin, eye, mucosal pain and irritation

155
Q

Define extravasation

A
  • Administration of IV infusions into the extravascular space/tissue around infusion sites
  • Can cause severe damage
156
Q

Which chemotherapies are potent vesicants upon extravasation?

A
  • Anthracyclines

- Vinca alkaloids

157
Q

Which chemo may cause pulmonary toxicity?

A

Bleomycin

158
Q

Which chemo may cause thromboembolism?

A

Thalidomide (immunomodulator)

159
Q

Which chemo may cause cardiotoxicity?

A

Doxorubicin (anthracycline)

160
Q

Which chemo may cause myelosuppression?

A

Carboplatin

161
Q

Which chemo may cause nephrotoxicity?

A

Cisplatin

162
Q

Which chemo may cause hypersensitivity reaction?

A

Asparaginase

163
Q

Which chemo may cause delayed wound healing?

A

Bevacizumab

164
Q

Which chemo may cause cerebellar toxicity?

A

Cytarabine (antimetabolite)

165
Q

Which chemo may cause neurotoxicity?

A

Vincristine (vinca alkaloid)

166
Q

Ways to avoid cardiotoxicity with anthracyclines?

A
  1. Limit lifetime doses

2. Use dexrazoxane

167
Q

What does the Philadelphia chromosome create?

A

BCR-ABL (over active tyrosine kinase)

168
Q

What are hormone sensitive cancers?

A
  1. Breast

2. Prostate

169
Q

What is imatinib MC used to treat?

A

CML

170
Q

What is thalidomide MC used to treat?

A

Myeloma

171
Q

What is asparaginase MC used to treat?

A

ALL

172
Q

What would 5-FU with leucovorin be used to treat?

A

Colon

173
Q

What would trastuzumab be used to treat?

A

Breast

174
Q

What would goserelin be used to treat?

A

Hormonal for prostate (androgen dependent) cancer

Pharm III - Exam 3 (2 decks)

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