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Pharmacology > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

Drugs causing mucositis

A

5-FU, Busulfan, Alkylating agents, Radiation

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2
Q

Palifermin

A

Drug that helps protect patients form severe oral mucositis, its a keratinocyte growth factor used with bone marrow transplants

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3
Q

Vesicants

A

Vinca alkaloids (warm compress), anthracyclines, nitrogen mustards

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4
Q

Dexrazoxane

A

Antidote for anthracycline extravasation. Give within 6 hours, binds to DNA topoisomerase II and locks it in a form that is no longer able to be affected. Acts as an iron chelator, minimizes oxidative damage caused by formation of anthracycline-iron complexes.

Cardio-protective with anthracyclines.

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5
Q

TLS

A

Hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia (calcium binds to phosphate, do not give calcium supplement or will precipitate calcium phosphate which can cause renal damage)

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6
Q

Allopurinol

A

Prevents the formation of uric acid by blocking xanthine oxidase, this in return elevates xanthine and hypoxanthine levels which cannot be monitored but also can precipitate.

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7
Q

Rasburicase

A

Induces uric acid breakdown. Caution with G6PD deficiency. Releases H2O2

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8
Q

G6PD deficiency

A

Seen in Middle East or Egyptian people, have trouble with oxidative stress and cannot tolerate the H2O2 released from uric acid breakdown, causes methemoglobinemia (oxygen can’t release from RBC)

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9
Q

Alkylating agents MOA

A

Chemical reaction with DNA (alkylation of DNA, RNA, proteins). When DNA starts to replicate and transcribe, it will identify the portion with the chemical reaction and will pause or replace the base with another base. This will create a nonsense mutation, it will no longer know what it is coding for.

CELL CYCLE NON-SPECIFIC. (Peak is important).

BIG ISSUE: will see secondary malignancy with these drugs, can replicate the wrong mutation instead of creating a nonsense mutation and dying. Most are AML and near impossible to treat.

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10
Q

Cyclophosphamide

A

Alkylating agent.

Pro-drug. Metabolized into a mustard compound that binds to DNA to alkylate it, and acrolein a toxic metabolite that causes hemorrhagic cystitis.

OPTIONAL: meson boluses (binds to acrolein). Pre-hydrate to water out the acid.

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11
Q

Ifosfamide

A

Alkylating agent.

HEMORRHAGIC CYSTITIS- always give meson.
Neurologic toxicity: treat with methylene blue. Will see encephalopathy.
Nephrotoxic.

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12
Q

Alkylating agents AE

A

Myelosuppression, dose related/cumulative. Nadir 7-14 days, duration 7-10 days.
Nausea, vomiting, stomatitis, diarrhea, anorexia.
Secondary malignancy.
Hemorrhagic cystitis.

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13
Q

Platinums MOA

A

Similar to alkylating agents, is an alkylating class (metal). Becomes a reactive platinum species and binds to DNA.

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14
Q

Platinum AE

A

Nephrotoxic: use amifostine to prevent. Hypomagnesia, hypocalcemia, hypokalemia
Myelosuppression: significant, worse with carboplatin
Peripheral neuropathies: worse with cisplatin
N/V: worse with cisplatin, acute and delayed
Ototoxicity
Cold sensitivity: oxaliplatin (vocal cord paralysis)

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15
Q

Cisplatin

A

Platinum agent

Peripheral neuropathy, n/v

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16
Q

Carboplatin

A

Platinum agent

Myelosuppression

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17
Q

Oxaliplatin

A

Platinum agent

Cold sensitivity

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18
Q

Temozolomide

A

Non-classical
Photosensitivity
VERY lipophilic: used for CNS involvement

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19
Q

Amifostine

A

Protective against nephrotoxicity with platinums

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20
Q

Antimetabolite

A

Drug that look like DNA or RNA bases that cause site mutations, must be present during S phase.

CELL CYCLE SPECIFIC.

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21
Q

Mercaptopurine

A 
6-MP. 
Purine analog (purines in DNA convert to uric acid). Metabolized by xanthine oxidase, if giving allopurinol must decrease 6-MP dose. Allopurinol prevents breakdown.
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22
Q

Fludarabine

A

Antimetabolite. Purine analog.
Causes lots of T cell suppression (cyclophosphamide also work on T cells)
Causes parathesias

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23
Q

Cytarabine

A

Ara-C, antimetabolite. Pyrimidine analog.
High doses can cause cerebellar toxicity, to monitor this make them sign their name daily, neuro checks.
Conjunctivitis, myelosuppression.

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24
Q

5-FU

A

Antimetabolite, pyrimidine analog.
Incorporates itself into RNA (replaces uracil). Normally uracil -> thymine by thymidylate synthetase. This does not recognize 5-FU, if flood the system will not produce thymine and no DNA produced.

FH4 involved in process of forming thymine (folinic acid). FH2 (folic acid) -> FH4 to make purines.

Some have deficiency in enzyme that breaks down 5-FU, only need 10% of dose. Will present with diarrhea, dehydration, myelosuppression.

Hand/foot syndrome: red/peeling
Mucositis, peripheral neuropathy, cardiotoxic, SEVERE DIARRHEA

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25
Q

Capecitabine

A

Oral 5-FU prodrug

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26
Q

Methotrexate

A

DHFR inhibitor. Blocks dihydrofluororeductase, necessary for the reduction that produces FH4 (folinic acid). Without this, there is NO purine synthesis. ALL DNA SHUTS DOWN, multi-organ failure.

Give leucovorin to replace FH4 to recover purine synthesis

DDI: sulfonamides

Immunosuppressant use

Myelosuppression, mucositis, renal toxicity (alkalinize urine for protection) cleared renally. Hepatotoxic, neurotoxic from high dose or IT.

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27
Q

Leucovorin

A

Folinic acid (FH4). Rescue for high dose-MTX. Increase 5-FU toxicity or enhances effects. 5-FU binds to thymidine synthase and folinic acid complexes, if you create more complexes it has more to bind to.

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28
Q

L-asparaginase

A

All cells have asparagine synthetase, some leukemic cells do not have adequate amounts. L-asparaginase enters the cell and breaks down asparagine to aspartic acid, shutting down leukemic cells.

Hypersensitivity seen.

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29
Q

Hydroxyurea

A

Inhibits formation of RNA bases, causes neutrophil suppression. Good for heavy tumor burden with leukemia, allows for safe treatment by tampering down leukemia cells prior to chemo.

For sickle cell anemia: increases fetal hemoglobin (doesn’t sickle), if you can keep this >20 won’t have crisis.

30
Q

Anthracyclines

A

Natural products. Inhibits topoisomerase II, free radical generation, DNA intercalation. Prior were antibiotics but too toxic. Anti-tumor drugs.

31
Q

Doxorubicin

A

Anthracycline. A liposomal drug affecting topoisomerase II (DNA affected). CELL CYCLE SPECIFIC: must be around during mitosis (30 min phase).

Anthracyclines have short half-lives, putting them in liposomal form lengthens this.

Solid tumors form new vessels (angiogenesis) that are very leaky, liposomes are small and fit through.

CARDIOTOXIC: lifetime cumulative dose of <450 mg/m2. Less with liposomal drugs. Dexrazoxane protects.
Vesicant
N/V
Myelosuppression
Discoloration of body fluids

Hepatic metabolism, once metabolized more cardiotoxic

Drug resistance

32
Q

Bleomycin

A

Anthracycline. Oxygen free radical, intercalation.

PULMONARY TOXICITY, follow PFTs

Renal elimination

Used with testicular cancer

33
Q

Mitotic Inhibitors

A

Vinca Alkaloids/Taxanes

Microtubule inhibitors, CELL CYCLE SPECIFIC (M PHASE)

34
Q

Vincristine

A

Vinca alkaloid. Block cell mitosis. Binds to tubulin, making it unable to aggregate and create microtubules. Microtubules pull DNA apart during mitosis.

Myelosuppression, peripheral neuropathy, constipation/ileus, SIADH, vesicant.

Hepatic metabolism: reduce dose if total bili >3 mg/dL

35
Q

Paciltaxel

A

Taxane. Mitotic inhibitor. Stops depolarization of microtubules, insoluble in water.

Neuropathy.
Allergic reaction: not to the drug but the vehicle carrying it.
Capillary leak: edema, pulmonary edema, third spacing a day or so after tx
**Pre-med with steroids: aids in hypersensitivity

36
Q

Chromatin Function Inhibitors

A

Epipodophyllotoxins, Camptothecins

37
Q

Etoposide

A

Epipo- topoisomerase II nihibitors (similar to anthracyclines). Topo 2 helps DNA unwind for replication.

Anaphylactic reaction, myelosuppression, secondary leukemia (seen fast, within 2 years)

38
Q

Irinotecan

A

Camp- topo I inhibitor, topo 1 cuts DNA during transcription causing single-stranded DNA.

*Releases Ach, within 4-6 hours can see lots of diarrhea (treat with atropine), after 24 hours it is osmotic related (treat with lomotil or loperimide).

Stomatitis, bone marrow suppression

39
Q

Monoclonal antibodies

A

New. Collect the short portion (antibody recognizing portion) from a mouse and place it onto a human antibody which are relatively all the same among humans.

LONG half-life of 3-4 weeks.

Kills antigens through T cell activation or compliment, this becomes an issue with T cell dysfunction.

40
Q

MOmab

A

Mouse.

41
Q

MUmab

A

Human.

42
Q

XImab

A

chimeric

43
Q

ZUmab

A

humanized

44
Q

Toxitumomab

A

Radioactive mab made by UofM

More toxic, infection risk, more labor

45
Q

Rituximab

A

Monoclonal antibody, chimeric

46
Q

Alemtuzumab (Campath)

A

mab, humanized.

Binds to CD52 which is present on B, T, NK, monocytes, macrophages, male reproductive tissue. Activates antibody-mediated cell lysis.

Prophylactic antibiotics required, high infection rate

47
Q

Gemtuzumab

A

mab, humanized

48
Q

VEGF

A

Growth factor responsible for angiogenesis.

49
Q

Bevacizumab (Avastin)

A

mab, blocks VEGF.

For lung, colon, breast cancer.

GI perforation, HTN, nephrotic syndrome (kidneys rely on angiogenesis), proteinuria, MI/CHF (can’t form new vessels), delayed wound healing

50
Q

Tyrosine kinase

A

HER family of growth receptors (epidermal growth factor)

51
Q

Trastuzumab

A

Humanized monoclonal antibody blocking HER2, inhibits fast proliferation.
High HER2 in 25% of breast cancers.
Will not kill the cancer.

ADDS TO CARDIOTOXICITY OF DOXO.

52
Q

Cetuximab

A

Blocks HER1
Treats metastatic colorectal cancer, approved for squamous cell carcinoma of the head and neck.

WILL SEE A RASH- THATS HOW YOU KNOW YOURE EFFECTIVELY TREATING. DO TREAT THE RASH.

53
Q

Small molecule TKI

A

Block tyrosine, can’t phosphorylate a protein (can’t be activated), can’t drive the cancer.

-NIBS

Oral, highly protein bound, 12-36 hour half-life.

54
Q

Imatinib

A

myelosuppression, fluid retention/edema (dose-related), nausea, diarrhea (all nibs), abdominal pain, musculoskeletal pain, myalgia, rash, hepatotoxic (severe)

55
Q

Erlotinib

A

HER1 inhibitor that blocks at small molecule

56
Q

Lapatinib

A

HER1 and HER2.
For breast cancer, metastatic or advanced tumors that overexposes HER2 and prior treatment with anthracycline, taxane, trastuzumab

57
Q

Sorafenib

A

Inhibits VEGF

For advanced renal cell carcinoma, unresectable hepatocellular carcinoma

58
Q

Sunitinib

A

VEGF at c-kit blockage

GI tumors with failure/intolerance to imatinib, advanced renal cell carcinoma

59
Q

Proteins as agents

A

Regulates tumor suppressor genes.
P53 is a tumor suppressor gene- if they have a mutation of this they have a poor outcome.
Some proteins can increase synthesis of tumor suppressor proteins and decrease the breakdown.

60
Q

Bortezomib

A

Blocks 26s proteasome which breaksdown proteins, specifically tumor suppressors

61
Q

5 Azacytidine

A

Methyl groups on DNA bases prevents DNA polymerase from binding. Normally have more methyl groups in front of oncogenes, so it binds more to tumor suppressors. With cancer this is reversed. More methylation = more tumor suppressor.

62
Q

Tamoxifen

A

Anti-estrogen, oral, approved for prophylaxis in high-risk.

HIGHER risk of thromboembolic events, hot flashes, dizziness, edema, endometrial cancer

63
Q

Aromatase inhibitors

A

Blocks conversion of estrogen. Blocks aromatase, blocking peripheral conversion of normal steroids into estrogen’s (post menopausal!)

64
Q

Anastrozole, Letrozole

A

Non-steroidal. Used for anti-estrogen resistant advanced breast cancer.
HIGHER risk of bone loss fractures and myalgia. Higher risk sexual dysfunction.
DO NOT suppress corticoid production

65
Q

Exemestane

A

Steroidal aromatase inhibitor

66
Q

LHRH agonist

A

Inhibit synthesis of sex steroids in both men and women, suppression of androgen synthesis
Used for prostate cancer
Too much LH will shut down pituitary, give testosterone blocker during the first week of treatment

67
Q

Leuprolide, Goserelin

A

LHRH agonist

68
Q

Progestational agents

A

Hormones, direct cytotoxicity. Decreases hormone dependent cancer cells, decreases estrogens effect.

Used as appetite stimulant, weight gain (most water related)
Only need 1/4 dose
Toxicities: glucocorticoid activity

69
Q

Megestrol acetate, Medroxyprogesterone

A

Progestational agents

70
Q

Flutamide

A

Non-steroid anti-androgen bloks androgen at receptor site. Used in combination at beginning of therapy with LHRH agent with prostate cancer.
Can see tachyphylaxis.
Hot flashes, impotence, drowsiness, depression, hepatotoxicity

71
Q

Glucocorticoids

A

Prednisone, Dexmethasone

Cytotoxic action with leukemia, lymphoma
Bind to steroid receptors in cytoplasm, binds to DNA in nucleus to transcribe genes. May interfere with glucose utilization.

Pharmacology (11 decks)

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