Week 14: Oncology Meds Flashcards

1
Q

Chemotherapy is best for those cancers with a high growth factor. What does this mean?

A

there ar emore proliferating cells than dying cells

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2
Q

Since chemo is effective on cells with high growth fractions (like cancer), what else can be effected?

A

High growth fraction normal cells:

Bone Marrow
Hair Follicles
Sperm Forming Cells
GI Epithelium

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3
Q

Solid tumors respond ___ to anti-cancer drugs

A

poorly (need debulking)

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4
Q

If solid tumors respond poorly to chemo, what does chemo help against?

A

metastasis or spreading cancer

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5
Q

What kinds of cancers respond best to drug therapy

A

disseminated cancers (high growth fraction) like leukemia and lymphoma

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6
Q

Why are CNS tumors hard to treat

A

the BBB prevents drugs from getting where the cancer is

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7
Q

What is the most effective way of tackling cancer via chemo

A

using multiple agents and attacking at different cell cycle stages

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8
Q

What are some commonly seen effects from anticancer drugs

A

Bone Marrow Depression (Neutropenia, Thrombocytopenia, Anemia)

Gi Issues

Hair Loss (Alopecia)

Sperm Forming Cell Issues (Sterility)

NV

Hyperuricemia

Vessel Injury from extravasation

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9
Q

Most traditional chemotherapeutic drugs interfere …

A

either with the synthesis of DNA, RNA, or proteins OR with the appropriate functioning molecules

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10
Q

How do cells die when someone has a chemo agent given

A

a proportion dies - thats why multiple doses are needed

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11
Q

Cell Cycle Specific Drugs

A

toxic to the cell at a particular phase and cause no significant harm during other phases

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12
Q

Cell Cycle Non Specific Drugs

A

kills cells regardless of their phase in the cell cycle - and are considered more toxic but stronger

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13
Q

Targeted Cancer Therapy

A

Newest chemo drugs that block the growth and spread of cancer by “Harnessing” bodys own immune system

Blocks signals that tell cancer cells to grow and divide uncontrollably

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14
Q

Advantage of Targeted Cancer Therapies

A

may be more effective and less harmful to normal cells

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15
Q

Prototype Cancer Chemotherapy/Oncology Drugs

A

9:

Cyclophosphamide (Cytoxan)
Methotrexate (Rheumatrex, MTX)
Mercaptopurine (Purinethol)
Fluorouracil (Adrucil)
Doxorubicin (Adriamycin)
Vincristine (Oncovin)
Cisplatin (Cisplatinum)
Paclitaxel (Taxol)
Tamoxifen (Nolvadex)
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16
Q

Cyclophosphamide (Cytoxin) Classification

A

ALKYLATING Chemotherapeutic Agent

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17
Q

Action of cyclophosphamide

A

Inactivation of DNA (via alkylation)

Binds to DNA to form cross links and prevent DNA, RNA, and protein synthesis

DNA Breakage will occur from alkylation

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18
Q

Is cyclophosphamide cell cycle phase specific or non specific

A

cell cycle phase non specific

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19
Q

What sort of cancers is cyclophosphamide used in

A

hematologic cancers and solid tumors

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20
Q

What happens when cyclophosphamide is metabolized by the liver

A

it turns into the cytotoxic agent against cancer cells (alkylation)

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21
Q

ADRs of Cyclophosphamide

A
  1. LEUKOPENIA (major one)
  2. Thrombocytopenia
  3. Hemorrhagic Cystitis (High Dose Therapy)

Other - Bone marrow depression, alopecia, amenorrhea, azoospermia, teratogenesis,hyperuricemia, NV

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22
Q

What is the lowest point of bone marrow depression with cyclophosphamide

A

nadir of WBC is between 9-14 days - most sensitive to infection but neupogen can help counteract this

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23
Q

What is hemorrhagic cystitis and how do we prevent it form occurring when taking cyclophosphamide?

A

It is bleeding inflamed bladder form high doses

we prevent by giving IV fluids and liberal amounts of fluid intake

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24
Q

What is length of cyclophosphamide therapy guided by?

A

It is guided by keeping leukocyte count between 3000-4000 mm^3

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25
Q

What other disease does cyclophosphamide help treat

A

rheumatoid arthritis (lower immune system to help)

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26
Q

Route of cyclophosphamide

A

IV or oral

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27
Q

Mesnex (Mesna)

A

a drug to help protect the bladder from high doses of cyclophosphamide

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28
Q

What is the issue with long term cyclophosphamide therapy

A

secondary cancers can occur like with other chemo drugs

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29
Q

Methotrexate (Rheumatrex, MTX) Classification

A

Antimetabolite Chemotherapeutic Agent ; Folate Antagonist

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30
Q

Action of Methotrexate

A

inhibits folic acid reduction, thereby interfering with synthesis of the coenzyme needed for DNA synthesis

S phase specific

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31
Q

Is methotrexate cell cycle phase specific or non specific

A

specific (S Phase)

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32
Q

Route of Methotrexate

A

Oral - for routine doses

IM - large doses

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33
Q

ADRs of Methotrexate

A
  1. STOMATITIS
  2. PULMONARY INFILTRATES AND FIBROSIS (In Lungs) (can permanently effect resp fxn)

Other: Leukopenia, Thrombocytopenia, Hepatotoxicity, NV, Alopecia, Tubular Necrosis (In Kidneys), HA, Gingivitis, Alopecia

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34
Q

What other disease can methotrexate be used on and why

A

Rheumatoid Arthritis - strong immunosuppressive effects inhibiting T Lymphocytes

Can also be used in Chrohns Disease soemtimes

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35
Q

Methotraxate is an anti-metbolite. What does this mean

A

it looks like folic acid to the body but is not

it will antagonize the receptors to stop cell DNA synthesis

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36
Q

Leucovorin

A

“Rescue” Folinic Acid

It is an antidote for methotrexate that can save normal body cells

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37
Q

Mercaptopurine (6-MP, Purinethol) Classification

A

Antimetabolite, Chemotherapeutic Agent, Purine Analog

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38
Q

Action of 6-MP / Mercaptopurine

A

Inhibits DNA synthesis by preventing purine incorporation into the DNA (antagonist)

S Phase Specific

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39
Q

Is 6-MP/Mercaptopurine cell cycle phase specific or non specific

A

Specific (S Phase_

40
Q

Route of 6-MP/Mercaptopurine

A

Oral - Readily

IV - an option

41
Q

ADRs of 6-MP/Mercaptopurine

A
  1. BONE MARROW DEPRESSION (Neutropenia, Thrombocytopenia, Anemia)
  2. JAUNDICE

Other: NV, anorexia, leukopenia, hyperuricemia

42
Q

Why do patients on 6-MP/Mercaptopurine develop Jaundice

A

It reflects liver damage

30% of patients on this drug develop hepatic dysfunction

43
Q

Fluorouracil (5-FU, Adrucil) Classification

A

Antimetabolite, Chemotherapeutic Agent, Pyrimidine Analog

44
Q

Action of Fluorouracil/5-FU

A

Affects specific steps in pyrimidine (Not purine) metabolism leading to inhibition of DNA and RNA synthesis

S Phase Specific

45
Q

Is 5-FU/Fluorouracil cell cycle phase specific or non specific

A

Specific (S Phase)

46
Q

What sort of cancer is 5-FU/Fluorouracil used for

A

solid tumors, esp. malignant GI tymors - can be used for other stuff as well though

47
Q

Route of 5-FU/Fluorouracil

A

IV (Oral is too unpredictable)

48
Q

ADRs of 5-FU/Fluorouracil

A
  1. MYELOSUPPRESSION (Anemia, Leukopenia, Thrombocytopenia) (Nadir 9-14 days)
  2. GI ULCERS
  3. ALTERATION IN TASTE

Other: Stomatitis, Diarrhea, Anorexia, NV, Alopecia, hand and foot syndrome

49
Q

What is the alteration in taste like with 5-FU

A

aversion to protein foods

50
Q

What are special situations for 5-FU/Fluorouracil use

A

PALLIATIVE TX: Breast, Colon, Rectal Cancer (Solid Tumors)

GI, Ovarian, bladder, Prostate, Pancreatic Carcinomas

Direct Hepatic Artery infusion for Liver Carcinoma or Metastasis

51
Q

What does antibiotic mean

A

one organism against another

its not just for infection - some products of streptomyces can help tx cancer

52
Q

Doxorubicin HCI (Adriamycin) Classification

A

Antibiotic Antitumor Agent ; Anthracycline

53
Q

Action of Doxorubicin HCl

A

Distorts DNA structure so synthesis of DNA and RNA is inhibited

54
Q

Is Doxorubicin HCl Cell cycle phase specific or nonspecific

A

non specific

55
Q

Route of Doxorubicin HCl

A

mostly given as IV infusion

56
Q

ADRs of Doxorubicin HCl

A
  1. ACUTE AND DELAYED CARDIOTOXICITY (dysrhythmias, EKG changes, cardiomyopathy, CHF and death)
  2. SIGNIFICANT BONE MARROW DEPRESSION
  3. RED/ORANGE URINE/TEARS

Other: Alopecia, NV, Stomatitis, Local Extravasation Risk

57
Q

What is important about the dosage of Doxorubicin HCl

A

once a person reaches maximum dosage they cannot have anymore and there needs to be careful calculation and administration due to the RISK FOR HEART DAMAGE that is great

58
Q

How is the bone marrow depression worse in Doxorubicin HCl

A

the neutropenia occurs at day 7 (earlier than most)

59
Q

What kind of cancers is Doxorubicin HCl used in

A

solid tumors or disseminated cancer

60
Q

Why does red colored food cause NV and anorexia with patients on Doxorubicin HCl

A

The drug is a dark cherry kool aid red color

This even turns your urine and tears red orange or red pink

61
Q

Doxorubicin HCl is a severe vesicant, what implication does this have on a patient

A

A vesicant can damage tissue permanently and since it is given IV, extravasation can lead to severe pain and tissue damage permanently (can lessen with an implanted port)

62
Q

Vincristine (Oncovin) Classification

A

Chemotherapeutic Agent; Vinca Alkaloid

63
Q

Action of Vincristine

A

binds specifically with the protein TUBALIN, part of cell microtubules

Blocks mitosis during metaphase so it is M phase specific and STOPS CELL DIVISION / MITOSIS

64
Q

Is Vincristine Cell Cycle Phase specific or non specific

A

Specific (M Phase)

65
Q

Route of Vincristine

A

IV (Oral unpredictable)

66
Q

ADRs of Vincristine

A
  1. NEUROTOXIC (peripheral neuropathy, muscle weakness, loss of deep tendon reflexes, HA, vocal cord paralysis, ptosis, diplopia, paralytic Ileus)

Other: GI disturbances, alopecia, only mild bone marrow depression

67
Q

What is unique about vincristine and bone marrow

A

it only causes mild bone marrow depression - to the point it is considered bone marrow sparring compared to other chemo drugs and thus can be used alongside them

68
Q

Vincristine is a ____ and can damage surrounding tissues

A

Vesicant

69
Q

What is vincristine very effective at doing in children

A

inducing remissions in acute leukemias

70
Q

Cis-Platinum (Cisplatin) Classification

A

Heavy Metal Chemotherapeutic Agent

71
Q

Action of cis-platinum

A

inhibits DNA precursors, maybe via alkylating effect

72
Q

Is cis-platinumcell cycle phase specific or non specific

A

Non Specific

73
Q

route of cis-platinum

A

ORAL, IV is ineffective

74
Q

ADRs of cis-platinum

A
  1. SEVERE NV
  2. NEPHROTOXICITY
  3. OTOTOXICITY

Other: Mild and transient bone marrow depression, peripheral neuropathy (tingling, numbness in fingers, toes and face)

75
Q

How ototoxic is cis-platinum

A

enough to cause loss of high frequency hearing

76
Q

What must be given alongside cis-platinum

A

other drugs such as anti-emetics to prevent potential significant side effects

77
Q

Since cis-platinum is a heavy metal, what must be done

A

a “mannitol flush” must be given before and after to prevent acute tubulular necrosis of the kidneys - get it moving through to prevent pain

78
Q

Paclitaxel (Taxol) Classification

A

(newer) Chemotherapeutic Agent (Taxane Family)

79
Q

Action of Paclitaxel

A

Inhibits normal dynamic reorganization of the microtubule network needed for vital mitotic cell fxns

(G2 and M phase specific)

So it works in prepartion for Mitosis causing problems there but begins working before that phase

80
Q

Is paclitaxel cell cycle phase specific or non specific

A

specific (works in G2 and M phase)

81
Q

Route of paclitaxel

A

IV

82
Q

ADRs of Paclitaxel

A
  1. SEVERE HYPERSENSITIVITY RXNs
  2. PERIPHERAL NEUROPATHY / NEUROTOXICITY
  3. MYELOSUPPRESSION

Other: bone marrow suppression (nadir of 11 days), CV bradycardia/heartblock/MI, arthralgia, GI NV/diarrhea/mucositis, alopecia, change in liver fxn

83
Q

What is unique about the alopecia with paclitaxel

A

it is very sudden and comes out in clumps

84
Q

Hypersensitivity reactions occur in __% of paclitaxel patients and needs what prior?

A

10%; pre medication with corticosteroids, diphenhydramine, and H2 antagonists

85
Q

Paclitaxel should not be given when

A

with neutrophil counts of <1500

86
Q

What sort of cancers may have paclitaxel given

A

ovarian

lung

breast

other

87
Q

Taxmoxifen (Nolvadex) Classification

A

Antiestrogen (competitive antagonist) , SERM (Selective Estrogen Receptor Modulator)

88
Q

Action of taxmoxifen

A

Competitive antagonist of estrogen

Binds to estrogen receptors to prevent stimulation of the receptors by estradiol (naturally occurring estrogen)

Because of this the estrogen cannot feed the cancer

89
Q

Route of taxmoxifen

A

oral

90
Q

ADRs of taxmoxifen

A

MOST NOT TROUBLESOME - TOLERATED WELL:

  1. MENSTRUAL IRREGULARITIES
  2. BONE PAIN (positive sign not bone cancer)
  3. ENDOMETRIAL CANCER POTENTIAL

Common: NV, Hot flashes

Other: Pruritis vulvae, increased tumor pain

91
Q

What is the most widely prescribed anti-cancer agent in the world

A

taxmoxifen

92
Q

What is taxmoxifen used for

A

to treat AND prevent breast cancer in high risk women (Adjunct to radiation, chemo and surgery)

93
Q

What is needed for taxmoxifen to be effective

A

the target tumor cells must be estrogen receptor (ER) positive

94
Q

Since taxomoxifen is a SERM, what effects may it have other than prevent tumor growth?

A

Agonist effects on tissues like the uterus, bone, and some other areas

Antagonist effects in areas like the breast

95
Q

What does the agonist effect of SERMs like taxomoxifen lead to in bone and the uterus

A

Uterus - Endometrium Cancer potentially

Bone - Bone pain (good though sign)

96
Q

What is the max amount of time taxmoxifen is used and why

A

5 years - want to prevent causing endometrial cancer