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Clinical 2 (Part B) > 20 - Cancer Treatment > Flashcards

20 - Cancer Treatment Flashcards

1
Q

Adjuvant therapy

A

systemically administered therapy with cytotoxic drugs, hormones, or biologic response modifiers to kill micro metastases after the primary tumor has been eliminated

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2
Q

Neoadjuvant therapy

A

treatment given before surgery to reduce tumor and allow better surgical resection

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3
Q

Remission

A
  • complete disappearance of cancer symptoms, typically occurring when the number of cancer cells decrease below 10^9.
  • complete clinical remission is not the same as being cured
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4
Q

Cure

A

to be rendered clinically and pathologically free of disease, and returned to a life expectancy the same as that of a healthy individual of the same age and sex

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5
Q

What are factors that determine treatment modality ?

A
  • Cancer type
  • Location and size of tumor
  • Extent of disease
  • Radiosensitivity or chemrsensitivity
  • History of prior therapy
  • Concurrent organ dysfunction
  • Performance status (overall physical functioning)
  • Patients goals/wishes
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6
Q

What are cancer treatment modalities ?

A
  • Surgery
  • Radiation therapy
  • Chemotherapy (targets any cell that is growing quickly)
  • Biological & Targeted Therapy
  • Supportive care
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7
Q

What are some of the roles that surgery can play in cancer management?

A
  • Can provide curative Tx for localized mass
  • Can be used to reduce the size of the tumor, or debulk it
  • Can be used to remove isolated metastatic disease (ex. pulmonary wedge resection)
  • Can be used to treat complications such as obstruction, hemorrhage, or perforation
  • Can be used to reconstruct anatomic defects to improve function or appearance
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8
Q

How does radiation therapy work?

A
  • Breaks bonds in DNA causing loss of proliferative capacity
  • Induces apoptosis
  • Plan to deliver tumoricidal dose within limits of tolerance of surrounding normal tissues
  • Normal tissues are usually able to recover better than cancer cells
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9
Q

What are some methods of delivery of radiation therapy?

A
  • External beam (tele therapy)
  • Internal (brachytherapy)
  • High dose rate (HDR) with remote loading
  • Low dose rate implanted (temporary or permanent)
    ex. prostate seeds
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10
Q

What are some general radiation SE ?

A
  • radiodermatitis
  • fatigue
  • weight loss d/t anorexia
  • myelosuppression (skull, sternum, long bones)
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11
Q

What are some site specific radiation SE ?

A

depends on structures present in area of radiation Tx (RTx)

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12
Q

What is pulmonary pneumonitis?

A

can be acute or develop 2-3 months after tx starts

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13
Q

What is pulmonary fibrosis?

A

occurs after 6-12 months, chronic, not reversible, can be fatal

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14
Q

For pulmonary, what do we need to assess?

A

cough, fever, hypoxia, exertion dyspnea

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15
Q

Treatment for pulmonary radiation therapy?

A
  • High-dose corticosteroids for acute pneumonitis
  • Bronchodilators
  • Oxygen (may need home O2 if chronic fibrosis)
  • activity modification
  • codeine is more effective cough suppressant than OTC
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16
Q

What are some GI side effects of radiation therapy and how can we manage them?

A

N/V:

  • prophylactic anti-emetics before tx
  • usually occurs if brain or stomach in tx field, otherwise is mild

Diarrhea:

  • Monitor intake/output, assess for dehydration & acidosis if severe
  • Non-irritating diet: low-fibre
  • Anti-diarrheal medications
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17
Q

How is sexuality/reproductive health affected by radiation therapy?

A
  • Gonads very sensitive to radiation
  • Easier to shield testicles from pelvic radiation
  • If one ovary spared, may preserve fertility

-Inform pt of expected effect of Tx on fertility

  • In Manitoba: Heartland Fertility Clinic offers:
  • egg, embryo, sperm cryopreservation
  • Patient pays
  • They prioritize cancer patient referrals
  • If gene radiation may develop dryness, atrophy
  • Lubricants, sexual activity/dilator to maintain vaginal patency

-Impotence r/t prostate cancer Tx

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18
Q

What is chemotherapy?

A
  • The use of cytotoxic medications to kill cancer cells
  • Goal: reduce and/or eliminate visible and invisible (micro metastases) disease
  • Cancer cells can develop resistance to chemo tx
  • Most often is SYSTEMIC, therefore systemic side effects
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19
Q

What are some routes of chemo administration?

A

Most common:

  • Oral
  • IV (bolus and then continuous infusion)
  • Intra-thecal: b/c most chemo doesn’t cross BBB (only certain drugs are ok via this route!)

Less common:

  • IM: L-asparaginase
  • Intra-cavitary: ex. bladder
  • SC: may be used for basal cell skin cancer
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20
Q

What are some principles of chemotherapy?

A
  • Start therapy when tumor burden is low and growth fraction is high
  • Use a combination of drugs
  • Use a dosing schedule that limits tumor regrowth during host tissue recovery
  • Dose to maximum tumor response or toxicity before changing therapy
  • Therapeutic benefit must exceed toxicity
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21
Q

What are some principles of combination chemotherapy regimens?

A
  • Drugs are active against the tumor when used alone
  • Drugs that have a biochemical basis for suspected synergy
  • Drugs that have different MOA
  • Drugs that produce toxicity in different organ systems (or in the case of bone marrow toxicity, the toxicity occurs at different times following administration)
  • Optimal dose and schedule for the agents are used
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22
Q

Combo Chemo:

R-CHOP

A
  • Rituximab
  • Cyclophosphamide
  • Hydroxydaunorubicin (doxorubicin)
  • Oncovin (vincristine)
  • Prednisone
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23
Q

Combo Chemo:

ESHAP

A
  • EtopoSide
  • metHylprednisolone
  • Ara-C (cytarabine)
  • cisPlatinum
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24
Q

Combo Chemo:

FEC

A
  • Flurouracil
  • Epirubicin
  • Cyclophosphamide
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25
Q

Combo Chemo:

FolFOX

A
  • Folinic acid (leucovorin)
  • 5-Flurouracil
  • OXalipatin
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26
Q

Doses of chemo are carefully calculated according to ?

A

body surface area

*height and weight on chemo patient must be exact & measured

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27
Q

What are some classifications of chemo agents?

A
  • Alkylating agents
  • Antimetabolites
  • Antitumor antibiotics
  • Plant alkaloids
  • Nitrosureas
  • Corticosteroids
  • Hormones
  • Miscellaneous
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28
Q

Describe alkylating agents

A
  • contain highly reactive ions on their chemical structure
  • in some cases they must be activated/converted in the body to create the highly reactive, positively charged ions
  • these positively charged ions react with electron-rich portions of the cell (proteins and DNA) to form strong chemical bonds thus leading to inhibition of DNA synthesis
  • cell cycle non-specific
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29
Q

What is an example of alkylating agent?

A

Cisplatin

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30
Q

Describe Cisplatin

A
  • Very important agent u sed for the Tx of testicular cancer, lung cancer, ovarian cancer, breast cancer
  • Considered one of the most emetogenic antineoplastics currently used
  • Has a role as radiation sensitizer
  • Significant toxicities, including renal, neuropathy, alopecia
  • Can display delayed n/v (can use anti-emetics)
  • Toxic to kidneys!
  • If they already have poor renal function, it will drive them into renal failure
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31
Q

MOA of Cisplatin (alkylating agent)

A
  • Cl ion gets replaced with water
  • It goes into nucleus and becomes very highly reactive molecule, attaches to one strand of DNA and then the other and forms a cross-link
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32
Q

Is Cisplatin or Carboplatin better ?

A

Cisplatin

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33
Q

Describe plant alkaloids

A

Derivatives of different types of plants

  • Vinca alkaloids
  • Taxanes
  • Camptothecin
  • Epipodophylltoxins

Usually block a particular enzyme or arrest the cell is some step of mitosis or cell division

Cell-cycle specific

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34
Q

Describe Vincristine

A
  • Vinca alkaloid
  • Cell-cycle specific-inhibition of microtubule formation
  • Peripheral and autonomic neuropathy
  • Useful agent for the Tx of non-Hodgkin’s lymphoma
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35
Q

MOA of vincristine (plant alkaloids)

A

The mitotic spindle consists of helically polymerized tubulin

Vincristine incorporates intself into microtubules and prevents chromosomes from replicating

So it cannot undergo replication anymore

36
Q

Antimetabolites

A
  • Act by interfering with the metabolic processes of the cell. Interfere with nucleic acid biosynthesis
  • Are subdivided into folate antagonists, purine analogues, and pyridine analogues
  • As a class tend to bind enzymes responsible for DNA or RNA synthesis
  • Additionally may mimic one of the DNA or RNA nucleotides thus halting further replication
  • Cell-cycle specific
37
Q

_____ is an example of an anti-metabolite

A

flurouracil

38
Q

Describe Flurouracil (Antimetabolites)

A
  • Most extensively studied and used agent in colorectal cancer
  • Similar to the pyrimidine, uracil
  • Blocks the enzyme, thymidylate synthase
  • pattern of flurouracil toxicity differs between bolus administration and continuous infusion
  • Useful as a radiation sensitizer
39
Q

Describe antitumor antibiotics

A
  • drugs in this class are products of the species of bacteria Streptomyces
  • however, their bone marrow toxicity makes them inappropriate for use as antibacterial agents
  • anti-tumor antibiotics act by binding to or complexing with DNA and/or RNA, thus inhibiting replication - intercalation
  • can also produce single-strand and double-strand DNA breaks
  • can generate free radicals that will then seek out electron rich molecules such as DNA, RNA or proteins
  • cell-cycle non-specific
40
Q

An example of antitumor antibiotics ?

A
  • Doxorubicin (Adriamycin)

- Bleomycin

41
Q

Describe Doxorubicin (Antitumor antibiotic)

A
  • Anthracycline antibiotic with a lifetime cumulative dosage (500-550 mg/m2)
  • Most serious dose-limiting side effect is cardiomyopathy
  • Extensive use for Tx of breast cancer and lymphomas
  • Can produce radiation recall

*Cardiac toxicity is cumulative, need to record every dose they’ve ever gotten

42
Q

Describe Bleomycin (Antitumor antibiotic)

A
  • Damage DNA and prevent repair
  • Dose-limiting toxicity is pulmonary fibrosis
  • Active agent for the Tx of lymphomas, testicular cancer
  • Development of chills/fever post Tx
  • Cell cycle-specific
43
Q

Acute reactions of chemotherapy ?

A
  • Vomiting - prevent with anti-emetics

- Allergic reactions - some drugs require pre-medication to decrease risk of allergic rx/anaphylaxis

44
Q

Delayed effects of chemotherapy ?

A
  • Mucositis of varying severity
  • Alopecia
  • Bone marrow suppression: bleeding d/t decreased platelets
  • Fatigue: d/t decreased Hgb and other factors
  • Skin changes: dryness, flaking, peeling
  • N/V
  • Diarrhea
45
Q

What are some chronic toxicities of chemotherapy ?

A
  • Unique to each medication
  • Assess carefully to allow for early identification
  • Damage to: heart, kidney, liver, lungs, bone marrow, reproductive
46
Q

Toxicities to chemo:

Heart

A

Heart:
ex. anthracyclines - follow with serial MUGA, assess s/sx CHF, d/c meds if LV dysfunction. These meds have maximum lifetime doses even in absence of cardiac dysfunction

47
Q

Toxicities to chemo:

Kidney

A

Kidney:

-ex. cisplatin, carboplatin - monitor serum urea/Cr & CrCl (24 hour urine), monitor intake, output

48
Q

Toxicities to chemo:

Liver

A

Liver:

-ex. monitor LFTs, jaundice edema

49
Q

Toxicities to chemo:

Lungs

A

Lungs:

-ex. bleomycin - follow with serial PFTs, assess respiratory function

50
Q

Toxicities to chemo:

Bone marrow

A

Bone marrow:
-most drugs can cause chronic bone marrow failure if used over a prolonged period of time - follow with CBC and bone marrow Bx if signs of bone marrow failure

51
Q

Toxicities to chemo:

Reproductive

A

Sterility - depends on drugs & dose, assisted fertility

52
Q

What are some late effects?

A

Risk for leukemias and other secondary malignancies:
-Radiation and chemo Tx can induce DNA damage that can lead to new malignancies other than original Dx

Secondary malignancies other than leukemias have been reported:
-Includes breast (esp women who had chest radiation without shielding prior to 1980’s), uterine, thyroid, lung

Secondary malignancies are usually Tx-resistant

53
Q

What can lower neutrophils cause?

A

increased chance of infection and can die from infection

54
Q

What can lower platelets cause?

A

increased chance of bleeding

55
Q

List 2 types of hematopoietic therapy

A

1) Granulocyte Colony-Stimulating Factor (GCSF)

2) Erythropoietin

56
Q

Describe

1) Granulocyte Colony-Stimulating Factor (GCSF)

A

-Stimulates production, maturation, regulation, & activation of WBC
-Hastens recovery from bone marrow depression post-chemo
Stimulates stem cell mobilization to periphery for transplant
-Very important part of many protocols - revolutionized cancer care
-Supportive care not cancer Tx

57
Q

Describe

2) Erythropoietin

A
  • Used more commonly with renal disease than cancer
  • Platelet stimulating factors: none on market in Canada
  • Transfusions of RBC & platelets are use instead of growth factors
58
Q

What effect does Bleomycin, Doxorubicin, Mitoxantrone, MTX cause?

A

Mucositis

59
Q

What effect does Cytarabine, 5-FU cause?

A

Mucositis, Diarrhea

60
Q

What effect does high dose melphalan have?

A

Esophagitis, stomatitis, diarrhea, and colitis

61
Q

What effect does high dose Etoposide have?

A

oropharyngeal mucositis

62
Q

Describe CINV (chemotherapy-induced nausea and vomiting)

A
  • maximal emetic intensity seen within 24 hours post dose

- distinct second phase seen, occurring on days 2-4 post dose

63
Q

What are some factors relating to chemotherapy causing CINV ?

A
  • Intrinsic emetogenicity of chemotherapeutic agents
  • Dose
  • Route of admin
  • Rate of infusion
  • Repeated cycles of chemotherapy
64
Q

What are some factors relating to patients causing CINV ?

A

Patient characteristics:

  • Low alcohol consumption (<10 drinks/week)
  • Younger age (<50 years)
  • Female gender
  • History of motion sickness
65
Q

Cisplatin is a level 5 agent for ______

A

nausea

66
Q

List some antinauseants

A
  • Steroids (dexamethasone)
  • Dopamine receptor agents (haloperidol, domperidone, metoclopramide)
  • Serotonin antagonists (ondansetron, granisetron, dolasetron, palonesotron, tropisetron)
  • Benzodiazepines (lorazepam)
  • Cannabinoids (abilene, dronabinol)
  • Neurokinin-2 blockers (aprepitant)
67
Q

Describe pulmonary toxicity of antineoplastics

A

Pulmonary toxicity:

  • Rare but often fatal complication of cancer chemotherapy
  • Usually a result of inflammation and subsequent formation of scars in the lungs after the administration of certain chemotherapy drugs
  • Sometimes referred to as pneumonitis or pulmonary fibrosis
  • Dose-limiting toxicity of agents such as bleomycin, busulifan, carmustine
  • Concern if patient to receive chest irradiation
68
Q

List types of toxicities associated with antineoplastics?

A
  • pulmonary toxicity
  • peripheral neurotoxicity
  • cardiac toxicity
69
Q

Describe peripheral neurotoxicity of antineoplastics

A
  • Common dose-limiting toxicity of many of the plant alkaloid agents
  • Many times the damage appears to be dose dependent, and occasionally irreversible
  • Nerves that are affected are primarily the peripheral nerves, although cranial nerves and autonomic nerves can also be damaged
70
Q

Describe cardiac toxicity of antineoplastics

A
  • is a recognized dose-limiting toxicity of several agents
  • common with the anthracycline antibiotics (ex. doxorubicin, epirubicin, daunorubicin, idarubicin, mitoxantrone)
  • being seen with seam of the monoclonal antibodies
  • Risk factors for cardiac damage: age, pre-existing heart disease, concurrent treatment with cyclophosphamide, treatment schedule
71
Q

What is biological Tx ?

A
  • “uses living organisms, substances derived from living organisms, or synthetic version of such substances to treat cancer”
  • approved: monoclonal antibodies, cytokines
  • investigational: therapeutic vaccines, gene therapy, adoptive T-cell transfer
72
Q

What is targeted Tx ?

A
  • “drugs or other substances that block the growth & spread of cancer by interfering with specific molecules involved in tumor growth & progression”
  • “drugs that interfere with cell growth signalling or tumor between development, promote the specific death of cancer cells, stimulate the immune system to destroy specific cancer cells & deliver toxic drugs to cancer cells
73
Q

What was the first molecular target of endocrine Tx ?

A

estrogen receptors in breast cancer

74
Q

What are 3 types of endocrine treatment?

A
  • SERMs
  • Aromatase inhibitors
  • Hormonal agents: Bicalutamide
75
Q

SERMs

A

Selective estrogen receptor modulators (SERM’s):

-Tamoxifen

76
Q

Aromatase Inhibitors

A

Aromatase inhibitors:

  • Exemestane, anastrozole, letrozole
  • For post-menopausal women (pre-menopausal women produce enough on their own)
77
Q

Describe Hormonal agent (Bicalutamide)

A

Hormonal agents: Bicalutamide:

  • Useful for treatment or prostate cancer
  • Inhibit the translocation of the androgen receptor not allowing testosterone to bind
  • Useful in combination with gonadotropin-releasing hormone analogues
  • Oral medication
  • Major side effect is diarrhea
78
Q

Describe monoclonal antibodies for targeted therapy

A
  • Ab engineered to bind to specific targets on cell surface
  • IV
  • Also used for other illnesses (ex. RA, Crohn’s, psoriasis)
  • Risk of anaphylaxis with administration
79
Q

What are some SE of monoclonal antibodies ?

A
  • Fatigue
  • Capillary leak syndrome
  • Hepatotoxicity
  • Bone marrow suppression
  • CNS effects
  • Cardiac dysfunction
80
Q

What are some monoclonal antibodies ?

A
  • trastuzumab
  • cetuxiimab
  • rituximab
81
Q

What are some tyrosine kinase inhibitors?

A
  • Imatinib
  • Dasatinib
  • Nilotinib
82
Q

Angiogenesis

A

Tumor cells secrete VGEF to grow so this is a target to kill cancer cells

83
Q

What does Bevacizumab target?

A

-Monoclonal antibody that targets VEGF receptor and inhibits angiogenesis

84
Q

What are some oncologic emergencies?

A
  • FNE/Septic shock
  • Hypercalcemia of malignancy
  • TLS
  • SIADH (intra-vascular fluid excess)
  • DIC (simultaneous bleeding and clotting)
85
Q

Stem Cell Sources:

Allogeneic

A

Allogeneic: from a donor matched to recipient

  • Related: family, usually sibling
  • Unrelated: donor from one of the unrelated donor registries
86
Q

Stem Cell Sources:

Autologous

A

patient’s own stem cells removed, stores & reinfused

87
Q

Stem Cell Sources:

Syngeneic

A

identical twin donor

Clinical 2 (Part B) (30 decks)

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