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Q2 - Cancer Flashcards

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1
Q

Males are most effected by what top 3 cancer types?
Females?

A

Males - lung, prostate and colon/rectum
Females, Lung, breast and colon/rectum.

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2
Q

When is adjuvant chemo administered?
Neoadjuvant?
Induction chemo?
Consolidation chemo?
Myeloablative?
Maintenance?

A

Adjuvant = AFTER main tx
Neoadjuvant = BEFORE main tx
Induction = goal to induce remission
Consolidation = use after induction to target remaining cancer cells.
Myeloablative = HD to kill ca cells in bone marrow
Maintenance = prevent return of ca after it has disappeared following initial therapy.

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3
Q

What are the two principles of cytotoxic chemotherapy and how do they differ?

A

Log -kill = cytotoxic chemo good approx for leukemias and lymphomas (NOT solid tumors). More frequent scheduling and higher doses = more success.

Gompertzian = more appropriate for SOLID tumors. Surgical reduction of bulk tumor f./u with chemo

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4
Q

Immunotherapy has greatest benefit at 10^?

A

5

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5
Q

What happens during G1 cell cycle?
S?
G2?
M?

A

G1 = cell growth, protein growth and preparation of DNA synthesis
S = DNA synthesis
G2 = check for damaged DNA and synthesis of mitotic cellular components
M = mitosis (cell division)

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6
Q

What normal (non cancerous cells in the body) are rapidly dividing and can be targeted by cytotoxic chemo?

A

Bone marrow, hair follicles, mucosal lining, GI tract, skin and germinal cells.

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7
Q

Chemotherapy selection based on _____ and _______

A

Tumor/drug factors and patient factors.

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8
Q

One important thing to consider with combination chemo?

A

Sequence of agents - infuse certain agents before other agents to minimize AEs and SEs

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9
Q

What are the 5 main classes of cytotoxic agents? Which are non-cell-cycle specific (NCCS) and which are CCS?

A

TAA VAT
Alkylating agents (NCCS)
Tpoisomerase Inhibitors/anthracyclines (NCCS)
Antimetabolites(CCS)
Vinca Alkaloids (CCS)
Taxanes. (CCS)

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10
Q

Which classes of chemotaxis meds affect M phase. MOA?

A

Taxanes and vinca alkaloids
Microtubule inhibitors

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11
Q

What are the 1st chemotherapeutic? What cell cycle(s) do they mainly target? What is their MOA?

A

Alkylating agents
G1+S
Cross-links DNA at the guanine base so the strands can’t be unwound and replicated. Like a piece of yarn stuck in a zipper
Causes single or double strand breaks in tumor cell DNA.

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12
Q

Major ADRs with Platinum compounds?
Cyclophosphamide + ifosfamide?

A

Alkylating agent - cytotoxic chemo
N/v, renal/neurotox

Hemorrhagic cystitis w/high dose.

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13
Q

What meds cause hemorrhagic cystitis and how can we treat?

A

Cyclophosphamide, ifosfamide (nitrogen mustard alkylating agents)

Tx w/ Mensa.

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14
Q

Bendamustine, chlorambucil, cyclophosphamide, ifosfamide, mechlorethamine, melphalen are all ______

A

Nitrogen mustard alkylating agents

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15
Q

Cisplatin, carboplatin and oxaliplatin are all ________

A

Cytotoxic, alkylating platinum compounds.

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16
Q

Doxorubicin, Daurnorubicin, Idarubicin, Epirubicin, Mitoxantrone, Bleomycin, Mitomycin C and Dexrazoxane are all _________

A

Cytotoxic, anthracyclines

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17
Q

Anthracyclines MOA?

A

Topoisemerase II inhibitors (block the unwinding of DNA) = fragmentation and blocked synthesis of RNA/DNA.

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18
Q

What are some common SEs of Anthracyclines?

A

Myelosuppression, cardiotoxicity, N/v, Mucositis, Red/orange urine (like blood!

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19
Q

Which med is used to treat leukemia with underlying cardiac dysfxn? Class?

A

Dexrazoxane = anthracycine topoisemerase II inhibitors

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20
Q

What cell cycle do anthracyclines work?

A

M and S phase.

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21
Q

Many anthracyclines have red urine except?

A

Mitoxantrone - blue/green urine.

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22
Q

What is a AE of Bleomycin?

A

Pulmonary toxicity.

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23
Q

What types of cancers is Mitomycin used for?

A

GI tumors
Bladder cancer

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24
Q

What is another name for topoisomerase inhibitors?

A

Anthracyclines

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25
What are the classes of CCS cytotoxic agents?
Antimetabolites, vinca alkaloids and taxanes.
26
3 types of Antimetabolites? (Class?)
Antimetabolites are CCS cytotoxic chemos. Antifolates Pyrimidine Antagonists Purine Analogs
27
What are examples of Antifolate drugs? MOA?
Type of antimetabolite “-treated/trexed” Methotrexate Pemetrexed Pralatrexate MOA: inhibit DNA synth and repair by reducing purine, folate and thymidylate acid synth (needed for protein and DNA/RNA synth).
28
What medication is used in the treatment of relapsed or refractory t-cell lymphoma?
Pralatrexate - antimetabolite/Antifolate.
29
What are some examples of Pyrimidine antagonists? MOA?
Antimetabolites “-Tabine” Cyterabine, Gemcitabine, Flourouracil, Capecitabine MOA: incorporate false precursor in DNA/RNA through inhibition of proteins involved in nucleotide metabolism “Pyramid schemes are FALSE! “AH BEEN fooled!” :P
30
Examples of purine analogs? MOA?
Antimetabolite. “-bine/rine/nine” not to be confused with “-Tabine” Pyrimidine antagonists Mercaptopurine, Thioguanine, Fludarabine, Cladribine, Clofarbine MOA: 2 fold - inhibit ribonucleic reductive and stalling of DNA polymerization.
31
What cell-cycle phase(s) to Antimetabolites work in?
(Antifolates, Pyrimidine antagonists, and purine analogs) S phase specific.
32
What cell-cycle phase(s) do vinca alkaloids work in?
M-phase specific
33
What is the MOA for vinca alkaloids?
Antimicrotubule - block beta-tubular polymerization needed for cell division.
34
Vincristine, vinblastine and Vinorelbine are all ______
Vinca Alkaloids Antimicrotubule M-phase specific “Vin-“
35
What cell-cycle phase(s) do Taxanes target?
M-phase specific
36
Examples of Taxane agents? MOA?
“-taxel” Paclitaxel, docetaxel, cabazitaxel, Abraxane.
37
AEs with taxanes?
Myelosuppression + neuropathy.
38
Difference between Topoisomerase I and II inhibitors.
I = 1/2 strands cut, eukaryocytes only, no ATP, 3 subtypes II= 2/2 strands cut, eukaryocytes and prokaryocytes, ATP required, 2 subtypes
39
irinotecan and topotecan are _________ inhibitors
1 “Toucans have 1 big beak”
40
Etoposide and teniposide are _________ inhibitors
2 - “fast food take a LOT of energy to work of and comes with a choice of 2 sides” :P
41
What is the Mostellar equation?
An equation using body surface area to determine chemotherapy dose.
42
How is dose calculated for carboplatin
Area under the curve - CrCl and Calvert equation.
43
Most chemo uses actual body weight except for?
Carboplatin - uses AUC and CrCl
44
What class are chemotherapy agents under in regards to safety?
Class II
45
Route of administration for vincristine
IV piggy back VIncristine - IV
46
Vesicant drugs
“-icin” and “vin-“ Dacinomycin, Daunorubicin, Doxorubicin Epuribicin Idarubicin Mitomycin C Vinblastine Vincristine Vinorelbine
47
Most extravasation is treated by: What meds can treat extravasation?
Cold compress 15-20min 4x/day Hyaluronidase (sq) Dexrazoxane (IV) DMSO (topical)
48
Draw out “Chemo man” for common s/s
49
DOC for acute (w/in 24hrs) chemotherapy nausea/vomiting DOC for delayed n/v (1-5 days post chemo)
Ondansetron, palonosetron, aprepitant, fosaprepitant Dexamethasone.
50
Anticipatory nausea/v DOC DOC breakthrough or refractory n/v
Ativan Prochloperazine, promethazine and Olanzapine.
51
T/F: no treatment for mucositis. - prevention is best.
True
52
Pulmonary toxicity with these 2 drugs
Bleomycin, Busulfan.
53
What is the most common cause of chemo toxicity and dose reductions? Tx? AE?
Myelosuppression. Colony stimulating factor (CSF) Bone pain
54
Cardiotoxicity - what 2 drugs? Check what prior to tx?
Doxorubicin and daunorubicin Check baseline EF.
55
What kind of neurotoxicity can happen with taxanes? Vinca Alkaloids?
Impairment of fine motor skills, burning, numbness and tingling in hands and feet. Small sensory Ileus and paralysis of GI tract.
56
Agent for prevention and tx of acute chemo related diarrhea
Atropine 0.25-1mg IV or SQ Since chemo diarrhea is a Cholinergic rxn.
57
Tx of delayed chemo diarrhea?
Loperamide - 1st line Lomotil and octreotide = 2nd line.
58
Emergency meds for chemo anaphylaxis.
Benadryl, steroids, epi and albuterol.
59
What to do with chemo contaminated linen?
Wash twice.
60
Original “3 pillars” of cancer treatment modalities?
Cytotoxic chemo Surgery and radiation
61
“Novel” cancer treatment modalities
Stem cell/bone marrow transplant Immunotherapy Targeted Therapy Hormonal therapy.
62
What did William B Coley do?
Discovered that ca sometimes went away after severe infections.
63
3Types of cancer immunotherapy
Monoclonal Antibodies(mAbs) Checkpoint inhibitors Tyrosine kinase inhibitors
64
Suffixes of mAbs mean something: -Momab? -ximab? -Zumab? -mumab?
-momab. = all mouse -ximab = 30% mouse (chaimeric) -zumab = 90% humanized -mumab = 100% humanized (Xenomouse)
65
The -tu- in mAbs = ?
Attacks some type of TUmor.
66
Which monoclonal antibodies have the greatest hypersensitivity rxn risk?
Most mouselike Momab>ximab>zumab>mumab
67
T/F: you can rechallange patients with minor reactions to mAbs.
True. If the reaction is minor, stop the infusion, delay for 1-2 hours, pre medicate, and start again at a slower rate.
68
Which 2 meds cause an acne inform rash?
Cetuximab, panitumumab (MAbs)
69
What med causes impaired wound healing, hypertension, proteinuria?
Bevacizumab.
70
What type of cancer is cetuximab commonly used?
Head and neck ca.
71
How can we avoid the cetuximab skin rash?
Pre-treat with Doxy, sunscreen, hydration.
72
Check-point inhibitor examples and MOA?
PD1 Inhibitors: pembrolizumab, nivolumab, Cemiplimab PDL1 Inhibitors: Atezolizumab, Avelumab, Durvalumab CTLA-4 Inhibitors: Ipillimumab MOA: block the ca cell ability to “pass” for a normal cell.
73
Check-point inhibitors have a lot of _______-related SEs: for example:
Immune Any -itis possible! Colitis, Pneumonitis, Hepatis, Rash, Thyroiditis, nephritis
74
How are immune-mediated toxicities (related to check-point inhibitors) managed?
According to CTCAC scale Withhold drug Steroids until Grade 1 reached Resume immunotherapy with steroids
75
What does “pseudo-progression” mean and what therapy is it associated with? How can we distinguish this from real progression?
Check-point inhibitors. It gets worse before it gets better - don’t be fooled and stop the therapy if you see a temporary “progression” IL-8 testing (or other inflammation markers.
76
What is the MOA of TKIs?
Tyrosine Kinase is an integral part of many cell functions, such as: cell-signaling, growth, division, etc. If it is inhibited, then the ca cell will die.
77
Common TKI SEs/toxicities?
Rash and diarrhea, HTN and visual symptoms.
78
Common TKIs
“-tinib”
79
Dasatinib = TKI. SE?
Fluid retention can show up as SOB.
80
TKI Lapatinib SE?
Cardiotoxicity with reduced LVEF.
81
TKI Sunitinib SE?
Zebra hair.
82
What is the MOA of immunomodulators?
Induce cell-cycle arrest, inhibit angiogenesis and enhance t-cell and NK cell activity.
83
3 immunomodulators and common SEs?
“-lidomide” DVT -need prophy Peripheral neuropathy Do not take during pregnancy (birth defects)
84
MOA of hormonal therapy? Usually used________
Disrupt biologic hormone synthesis which disrupts the drive ca cells have. In combination with other cytotoxic or novel therapies
85
Common hormonal therapy meds and the cancers they treat. SEs?
Tamoxifen, Letrozole, Abiraterone, Enzalutamide Breast or prostate ca (makes sense cuz they’re HORMONAL) Hot flashes, reduced bone densities, increased DVT risk, fluid retention.

Pharmacology (20 decks)

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