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Oncology Midterm > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

Goals of Chemotherapy

A
  • Cure
  • Control (live with, like chronic illness)
  • Palliation (prevent suffering)
  • Neo-adjuvant treatment (before surgery)
  • Adjuvant treatment (after surgery)
  • Chemoprevention (hormone)
  • Myeloablation (preparation for BMT)
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2
Q

Adjuvant

A

in addition to

surgery > chemotherapy > radiation

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3
Q

Neo-adjuvant

A

chemotherapy > surgery > radiation

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4
Q

Concurrent

A

Surgery > (chemo + radiation)

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5
Q

Fundamental Principles of Chemotherapy

A
  1. Cell Killer model

2. Norton-Simon Hypothesis

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6
Q

Cell Killer Model

A

Skipper 1971
# of cancer cells killed per cycle (1st order kinetics)
Assumes all cells are: actively dividing, constantly treatment sensitive, growing at consistent rate
Limitations: not all actively dividing at same time, cells can grow at different rates
***doesn’t work

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7
Q

Norton-Simon Hypothesis

A 
Gompertzian Tumor growth kinetics
1977
Tumor grow faster when small???
Les time to recover, more likely to destroy
-dose-dense regimens
-shorter cycles
-more side effects (use growth factors)
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8
Q

Chemo Basics

A

-generally nonspecific (attack all dividing cells)
-Target rapidly dividing cells (cancer & healthy)
-cytotoxic
action during cell cycle
combination therapy = greatest effect

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9
Q

Cytotoxic

A

cellular poison

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10
Q

Cystostatic

A

blocks cell replication

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11
Q

cytocidal

A

apoptosis

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12
Q

Chemotherapeutic agents classification

A

cell cycle specific, nonspecific

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13
Q

Routes of Administration

A 
Oral
IV
IM
intra-arterial
Intrathecal
Intraperitoneal
Intrapleural
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14
Q

Intrathecal

A

NEVER VINCRISTINE

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15
Q

Cell Cycle

A

M, G1, S, G2….

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16
Q

Cell cycle Non-specific Drugs (CCNS)

A

exert effect within any cell cycle phase

Alkylating, Anti-tumor antibodies, nitrosureas, Hormones

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17
Q

Cell cycle specific drugs (CCS)

A

Exert effect within specific cell cycle phase

Antimetabolits, mitotic inhibitors (vinca, Taxanes), Topoisomerase I inhibitors, Topoisomerase II inhibitors

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18
Q

Alkylating Agents (CCNS)

A
  • cell cycle nonspecific
  • MOA: DNA strand breakage, prevent cell reproduction/replication
  • Alkylator classes
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19
Q

Common SE of Alkylating Agents

A 
myeolosuppresion
hypersensitivity
renal toxicities
GI
cutaneous toxicities (hand and foot)
secondary malignancies
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20
Q

Aklylating Agents CCNS: Platinum compounds

A
  • grouped with alkylating agents bc of mechanism of action
  • efficacy highly dependent on renal elimination
  • Adequate renal function IMPERATIVE
  • establish prior and during treatment (BUN and CREAT)
  • less likely to cause secondary malignancies
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21
Q

Antitimor Antibiotics: CCNS

A

different from those for infectiosn

  • MOA: Cell cycle nonspecific, bind with DNA and inhibit synthesis, prevents cell replication
  • produced by streptomyes organisms
  • Anthracyclines
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22
Q

Antitumor Abx - common SE

A

Myelosuppression
GI toxicities
Cutaneous toxicities - vesicants (doxorubicin) EMERGENCY
Organ toxicities (cardiotoxic, pulmonary toxic)

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23
Q

Anthracyclines

A

antitumor antibiotic
has lifetime maximum cumulative dose
too much will affect cardiac function

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24
Q

epipodophyllotoxins

A

Antitumor antibiotic classification

Topoisomerase II inhibitors

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25
Q

Bleomycin

A

Antitumor abx CCNS
pulmonary toxicity: fibrosis
fever and chills during and after infusions
lifetime dose limit 400

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26
Q

Doxorubicin

A 
red in color
vesicant
cardiac toxicity
Dexrazoxane (cardioprotectant) given together if possible
flare reaction
N/V
red urine
lifetime dose 550mg (reduce if prior irratidation or cotreat with cytoxan)
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27
Q

Nitrosoureas CCNS

A

cell cycle nonspecific
MOA: break DNA helix, inhibit replication
**crosses BBB (rare), treats brain tumors
highly lipid soluble
treats cancers involving CNS (HL and NHL)

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28
Q

Notrosoureas SE

A

myelosuppression deyated, severe, and prolonged
GI toxicities: severe N/V, require antiemetics
secondary malignancies such as acute leukemia, bone marrow dysplasia
delayed pulmonary dmage
ex: Carmustine, Lomustine

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29
Q

Carmustine (BCNU)

A 
(Nitrosureas CCNS)
myelosuppression - nadir day 14, delayed
irritant
painful during infusion
pulmonary fibrosis
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30
Q

Lomustine

A 
(Nitrosureas CCNS)
Myelosuppression, nadir 14-21
given Q6-8 weeks to delay toxicities, time to recover
N/V
renal and hepatic toxic
pulmonary suppression
ovarian and sperm suppression
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31
Q

Hormonal Therapy

A

Anti-estrogen
Anti-Estrogen Aromatase Inhibitor
Lutenizing Hormone-releasing hormone analog
Anti-androgens

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32
Q

Breast tumor tissue tested for:

A 
Estrogen Receptors (ER)
Progesteron Receptors (PR)
*can use hormonal treatment if responsive
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33
Q

ER/PR positive tumors

A

50-60% response rate with hormonal therapy

34
Q

Hormonal treatment: Premenopausal women

A

ovary = primary source of estrogen
ablation if estrogen source: oophorectomy, ovarian radiation, lutenizing hormone-releasing hormone antagonist,not been shown to benefit women receiving chemo, addition of hormonal agents are more effective

35
Q

Hormonal Treatment: Postmenopausal women

A

adrenal gland = primary source of estrogen is the adrenal glands
ablation of estrogen source - administering an aromatase inhibitor

36
Q

(Br ca hormonal trx) Anti-Estrogen Treatment

A

Tamoxifen (non-steroidal anti-estrogen)

  • oldest and most frequent
  • adjuvant therapy and advanced disease treatment
  • reducing risk of developing br ca in women at high risk
  • agonist or stimulator in endometrial tissue, bone, and lipids results in: inc blood close/endometrial cancer
37
Q

(Br ca hormonal trx) Anti-Estrogen Aromatase inhibitors (AIs)

A
  • suppress postmenopausal estrogen synthesis
  • inhibits peripheral conversaion of androgens to estrogens
  • ovarian production of estrogen is NOT affected
  • IMPORTANT: AIs are not indicated in premenopausal women
38
Q

(Br ca hormonal trx) Luteinizing hormone releasing hormon (LHRH) agonists

A
  • synthetic analogs of naturally occurring hormone
  • cause initial inc in testosterone levels bc stimulate LH release
  • pituitary gland becomes desensitized with continued use, results in significant decrease of estrogens and androgen production
39
Q

Prostate Cancer Hormonal Therapy

A

LHRH agonists

Antiandrogens

40
Q

Prostate hormonal therapy: LHRH

A
  • -synthetic analogs of naturally occurring hormone
  • cause initial inc in testosterone levels bc stimulate LH release
  • pituitary gland becomes desensitized with continued use, results in significant decrease of estrogens and androgen production
41
Q

Prostate hormonal therapy: Anti-Androgens

A
  • indicated for males with hormone-responsive metastatic prostate ca.
  • alone or in combo with gonadotropin-releasing hormone analog
  • bind to androgen receptor
  • block the effects of dihydrotestosterone on prostate cancer cells
42
Q

Side effects of hormonal therapy

A

Hot flashes

Osteopenia

43
Q

Management of hot flashes

A

Dec consumption of caffeine, alcohol and spicy foods
wear cotton
stress reducing activities
exercise
clonidine oral or transdermal patch (not proven)
neuroleptic agents and SSRI

44
Q

Management of osteopenia

A

occurs with most hormonal (except tamoxifen and raloxifene)

  • assess for family hx of osteoporosis or osteopenia
  • assess wt, race and exercise patterns
  • testing bone density annually
  • advise to avoid alcohol and smoking
  • perform weight bearing exercise
  • Vit D and calcium supplementation
45
Q

Side effects of hormonal therapy

A

Sexual Side effects
–women: vaginal dryness/atrophy (manage with lube)
–men: loss of libido, impotence, difficult topic to address
Cardiovascular effects: arterial lipid accumulation, promotion of blood flow, and vascular elasticity
Cognitive impairements

46
Q

Management of cardiovascular SE of hormonal therapy

A

assessing for smoking
hypertension
encourage exercise
checking and annual lipid profile

47
Q

Antimetabolites CCS

A

-Analogues of naturally occurring metabolites

MOA:

48
Q

Antimetabolites CCS Common side effects

A

Myelosuppresion
GI toxicities
Cutaneous toxicities (mucositis, hand/foot syndrome)

49
Q

Flourouracil (5FU)

A

?

50
Q

Capecitabine

A

?

51
Q

Methotrexate

A

Large dose range
renal failure can occur with large doses
Rescue with Leucovorin = antidote

52
Q

Mitotic Inhibitors (CCS)

A

cause neuropathy, may be lifelong - limit amount given
stops mitosis in M phase
can damage cell in G2 and S phases, keeps enzymes from making proteins needed for cell reproduction
Types:
Plant Alkaloids (Taxanes, Vinca alkaloids)
Epthilones
Estramustine

53
Q

Mitotic Inhibitors: Vinca Alkaloids (CCS)

A 
plant alkaloids
MOA: acts late G2 and M phase
Ex. Vincristine, Vinblastine, inorelbine
SE: myelosuppression, neuropathy, constipation, 
DEATH IF INTRATHECAL
54
Q

Mitotic Inhibitors: Taxanes (CCS)

A

plant alkaloid
MOA: Act in G2 and M phase
Paclitaxel: hypersensitivity, premed with dexamethasone, cimetidine, diphenhydramine, non-PVC bag with filter, perhipheral neuropathy, alopecia
Docetaxel: premed with steroids to reduce fluid retention, nail changes, lacrimation

55
Q

CCS Plant Alkaloids

A

CCS: M, G2, S
MOA: mitotic spindle poison, affects microtubule assembly, inhibits mitosis
Common SE: myelosuppression, alopecia, hypersensitivity, Neuropathy, constipation
Categories: Taxanes, Vinca alkaloids, epipodophyllotoxins

56
Q

Topoisomerase Inhibitors CCS

A 
Cell cycle specific: S, G2
interfere with enzymes (topoisomerases)
inhibits unraveling of DNA
prevents DNA replication during S and G2
grouped by type of enzyme they affect:
---Topoisomerase I inhib: campothecins
---Topoisomerase II inhib: Epipodophyllotoxins
57
Q

Topoisomerase I Inhibitors(CCS): Camptothecins

A

Cell cycle - S phase
MOA:
Irinotecan – cramping, Diarrhea, imodium or atropine, IV K support
Topotecan – diarrhea, alopecia, myelosuppresion

58
Q

Topo II Inhibitors (CCS): Epipodophyllotoxins

A

Plant alk.
G2, S,
MOA: induces irreversible blockade of cells, premitiotic, interferw with topo II enzyme rxn
Ex: Etoposide

59
Q

Factors affecting Response

A
  • combination vs single agent
  • combo therapy increases proportion of cells killed at any one time due to heterogeneous cell populations
  • reduces drug resistance
  • must have proven efficacy as single agents with minimally overlapping organ toxicity
  • uses drug synergy to maximize effect
60
Q

Factors Affecting response: Dose intensity

A

refers to amount of drug delivered per unit of time (mg/m2/wk)
dose delays or reductions have been shown to compromise survival
receiving less than 85% of planned dose may affect pts outcome

61
Q

Factors Affecting response: Dose Density

A

refers to reducing time between doses
give drugs in fractions that are closer together in time
lessen the chance of tumor regrowth between treatments
hematopoietic growth factors are usually required with dose-dense therapy or given prophylactically

62
Q

Factors Affecting response: Dose intensification

A

accelerated dose intensity treatment (ie. increasing doses over shorter periods of time)

63
Q

Factors Affecting response

A

Tumor burden
Resistance -
- anatomic failure agents unable to prenetrate sites like the brain, testes, or can occur because of inadequate blood supply
-genetic resistance caner cells may have a phenotypic, intrinsic type of drug resistance that arises from spontaneous mutations
+Characteristic: size and location
+physical status of pt
+psychosocial status of pt
+hormone receptor status -antihormonal agents can suppress the growth if tumor grows more rapidly in presence of certain hormones

64
Q

Mutations

A
  • cancer cells exposed repeatedly to chemotherapy may develop resistance by mutating
  • overexpression of MDR-1 gene (multidrug resistance)
  • MRD-1 overexpressed = pump overactive ad more chemotherapy is carried out than normal
  • Detection of MDR-1 gene product is a predictor of poor prognosis and survival
  • other genes: p53, BCL-2 and BAX
65
Q

Education Assessment

A 
primary language
patient understanding
barriers to learning
learning needs
knowledge of planned treatment
contact information
66
Q

Pretreatment: Review of treatment plan

A 
check height/weight BSA
calculate dose
check lab values
know vesicant or irritant properties
identify possible side effects and toxicities
67
Q

Pretreatment Assessment

A 
previous treatment
previous cycles, toxicities?
medical and surgical treatment
allegy hx
accurate height and weight BSA
lab values
performance status
tumor type, grade, and stage
68
Q

Pretreatment Risk assessment

A

physiologic versus chronologic age
performance/functional status (ability to perform ADLs and be independent)
comprehensive geriatric assessment
Comorbidities (esp. those affecting organs to be stressed by chemotherapy regimen: cardiac, renal, pulmonary, hepatic)

69
Q

Intra-cycle patient monitoring

A 
common chemo adverse effects and timing
acute, delayed and anticipatory CINV
mucositis
myelosuppression
fatigue
neuropathy
psychosocial distress
70
Q

Dose Modifications: delay dose

A

allow pt additional time to recover

may attempt to challenge at same dose after break

71
Q

Dose modification: Dose reduction

A

either on time, or after a break

once reduced, new lower dose level is generally permanent

72
Q

Dose modification: avoid

A

in cases where the full dose intensity is known to be associated with potential cure, avoid modifications

  • early stage breast cancer
  • germ cell tumor (testicular, ovarian)
73
Q

Chemoprotectants

A

Amifostine
Dexrazoxane
Mesna
Leukovorin

74
Q

Amifostine

A

chemoprotectant, reduces renal injury with chemo

75
Q

Dexrazoxane

A

cardioprotectant

76
Q

Mesna

A

used to decrease bladder irritation (hemorrhagic cystitis) with high dose chemo (ifosfamide)

77
Q

Leukovorin

A

used with methotrexate as a rescue

78
Q

Considerations for the NP

A

Assessment of patient capacity: ability to tolerate, social support
NP is the “shepherd”

79
Q

White Blood Cell suppot

A

Neupogen (shot acting), given until counts recover

Neulasta (long acting) - 24 hrs post chemo

80
Q

Red blood cell support

A

Epogen given weekly to every 3 weeks

Oncology Midterm (4 decks)

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