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Pharmacology > Q2 - Cancer > Flashcards

Q2 - Cancer Flashcards

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
Q

What are the classes of CCS cytotoxic agents?

A

Antimetabolites, vinca alkaloids and taxanes.

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26
Q

3 types of Antimetabolites? (Class?)

A

Antimetabolites are CCS cytotoxic chemos.
Antifolates
Pyrimidine Antagonists
Purine Analogs

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27
Q

What are examples of Antifolate drugs? MOA?

A

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).

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28
Q

What medication is used in the treatment of relapsed or refractory t-cell lymphoma?

A

Pralatrexate - antimetabolite/Antifolate.

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29
Q

What are some examples of Pyrimidine antagonists?
MOA?

A

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

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30
Q

Examples of purine analogs? MOA?

A

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.

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31
Q

What cell-cycle phase(s) to Antimetabolites work in?

A

(Antifolates, Pyrimidine antagonists, and purine analogs)
S phase specific.

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32
Q

What cell-cycle phase(s) do vinca alkaloids work in?

A

M-phase specific

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33
Q

What is the MOA for vinca alkaloids?

A

Antimicrotubule - block beta-tubular polymerization needed for cell division.

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34
Q

Vincristine, vinblastine and Vinorelbine are all ______

A

Vinca Alkaloids
Antimicrotubule
M-phase specific
“Vin-“

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35
Q

What cell-cycle phase(s) do Taxanes target?

A

M-phase specific

36
Q

Examples of Taxane agents?
MOA?

A

“-taxel”
Paclitaxel, docetaxel, cabazitaxel, Abraxane.

37
Q

AEs with taxanes?

A

Myelosuppression + neuropathy.

38
Q

Difference between Topoisomerase I and II inhibitors.

A

I = 1/2 strands cut, eukaryocytes only, no ATP, 3 subtypes

II= 2/2 strands cut, eukaryocytes and prokaryocytes, ATP required, 2 subtypes

39
Q

irinotecan and topotecan are _________ inhibitors

A

1
“Toucans have 1 big beak”

40
Q

Etoposide and teniposide are _________ inhibitors

A

2 - “fast food take a LOT of energy to work of and comes with a choice of 2 sides” :P

41
Q

What is the Mostellar equation?

A

An equation using body surface area to determine chemotherapy dose.

42
Q

How is dose calculated for carboplatin

A

Area under the curve - CrCl and Calvert equation.

43
Q

Most chemo uses actual body weight except for?

A

Carboplatin - uses AUC and CrCl

44
Q

What class are chemotherapy agents under in regards to safety?

A

Class II

45
Q

Route of administration for vincristine

A

IV piggy back

VIncristine - IV

46
Q

Vesicant drugs

A

“-icin” and “vin-“
Dacinomycin, Daunorubicin, Doxorubicin
Epuribicin
Idarubicin
Mitomycin C
Vinblastine
Vincristine
Vinorelbine

47
Q

Most extravasation is treated by:
What meds can treat extravasation?

A

Cold compress 15-20min 4x/day

Hyaluronidase (sq)
Dexrazoxane (IV)
DMSO (topical)

48
Q

Draw out “Chemo man” for common s/s

A
49
Q

DOC for acute (w/in 24hrs) chemotherapy nausea/vomiting

DOC for delayed n/v (1-5 days post chemo)

A

Ondansetron, palonosetron, aprepitant, fosaprepitant

Dexamethasone.

50
Q

Anticipatory nausea/v DOC

DOC breakthrough or refractory n/v

A

Ativan

Prochloperazine, promethazine and Olanzapine.

51
Q

T/F: no treatment for mucositis. - prevention is best.

A

True

52
Q

Pulmonary toxicity with these 2 drugs

A

Bleomycin, Busulfan.

53
Q

What is the most common cause of chemo toxicity and dose reductions?
Tx?
AE?

A

Myelosuppression.

Colony stimulating factor (CSF)

Bone pain

54
Q

Cardiotoxicity - what 2 drugs? Check what prior to tx?

A

Doxorubicin and daunorubicin
Check baseline EF.

55
Q

What kind of neurotoxicity can happen with taxanes?
Vinca Alkaloids?

A

Impairment of fine motor skills, burning, numbness and tingling in hands and feet.

Small sensory
Ileus and paralysis of GI tract.

56
Q

Agent for prevention and tx of acute chemo related diarrhea

A

Atropine 0.25-1mg IV or SQ
Since chemo diarrhea is a Cholinergic rxn.

57
Q

Tx of delayed chemo diarrhea?

A

Loperamide - 1st line
Lomotil and octreotide = 2nd line.

58
Q

Emergency meds for chemo anaphylaxis.

A

Benadryl, steroids, epi and albuterol.

59
Q

What to do with chemo contaminated linen?

A

Wash twice.

60
Q

Original “3 pillars” of cancer treatment modalities?

A

Cytotoxic chemo
Surgery and radiation

61
Q

“Novel” cancer treatment modalities

A

Stem cell/bone marrow transplant
Immunotherapy
Targeted Therapy
Hormonal therapy.

62
Q

What did William B Coley do?

A

Discovered that ca sometimes went away after severe infections.

63
Q

3Types of cancer immunotherapy

A

Monoclonal Antibodies(mAbs)
Checkpoint inhibitors
Tyrosine kinase inhibitors

64
Q

Suffixes of mAbs mean something:
-Momab?
-ximab?
-Zumab?
-mumab?

A

-momab. = all mouse
-ximab = 30% mouse (chaimeric)
-zumab = 90% humanized
-mumab = 100% humanized (Xenomouse)

65
Q

The -tu- in mAbs = ?

A

Attacks some type of TUmor.

66
Q

Which monoclonal antibodies have the greatest hypersensitivity rxn risk?

A

Most mouselike

Momab>ximab>zumab>mumab

67
Q

T/F: you can rechallange patients with minor reactions to mAbs.

A

True. If the reaction is minor, stop the infusion, delay for 1-2 hours, pre medicate, and start again at a slower rate.

68
Q

Which 2 meds cause an acne inform rash?

A

Cetuximab, panitumumab
(MAbs)

69
Q

What med causes impaired wound healing, hypertension, proteinuria?

A

Bevacizumab.

70
Q

What type of cancer is cetuximab commonly used?

A

Head and neck ca.

71
Q

How can we avoid the cetuximab skin rash?

A

Pre-treat with Doxy, sunscreen, hydration.

72
Q

Check-point inhibitor examples and MOA?

A

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
Q

Check-point inhibitors have a lot of _______-related SEs: for example:

A

Immune

Any -itis possible!
Colitis, Pneumonitis, Hepatis, Rash, Thyroiditis, nephritis

74
Q

How are immune-mediated toxicities (related to check-point inhibitors) managed?

A

According to CTCAC scale

Withhold drug
Steroids until Grade 1 reached
Resume immunotherapy with steroids

75
Q

What does “pseudo-progression” mean and what therapy is it associated with? How can we distinguish this from real progression?

A

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
Q

What is the MOA of TKIs?

A

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
Q

Common TKI SEs/toxicities?

A

Rash and diarrhea, HTN and visual symptoms.

78
Q

Common TKIs

A

“-tinib”

79
Q

Dasatinib = TKI. SE?

A

Fluid retention can show up as SOB.

80
Q

TKI Lapatinib SE?

A

Cardiotoxicity with reduced LVEF.

81
Q

TKI Sunitinib SE?

A

Zebra hair.

82
Q

What is the MOA of immunomodulators?

A

Induce cell-cycle arrest, inhibit angiogenesis and enhance t-cell and NK cell activity.

83
Q

3 immunomodulators and common SEs?

A

“-lidomide”
DVT -need prophy
Peripheral neuropathy
Do not take during pregnancy (birth defects)

84
Q

MOA of hormonal therapy? Usually used________

A

Disrupt biologic hormone synthesis which disrupts the drive ca cells have.
In combination with other cytotoxic or novel therapies

85
Q

Common hormonal therapy meds and the cancers they treat. SEs?

A

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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