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Oncology > Treatment of Cancer > Flashcards

Treatment of Cancer Flashcards

1
Q

4 phases of cell cycle?

A

G1 phase: RNA and protein synthesis, cell growth, DNA repair
S phase: DNA completely replicated
G2 phase: additional synthesis of RNA, protein and specialized DNA
M phase: mitosis

  • resting phase: cells don’t engage in synthetic activities
  • growth fraction: proportion of cells in tumor actively involved in cell division
  • generation time: length of cell cycle
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2
Q

Mode of action of Chemo?

A
  • cell cycle specific:
    kills in specific phase of cell cycle, most useful in tumors with large proportion of actively dividing cells
  • cell cycle nonspecific:
    kills in all phases, useful in tumors with low growth index
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3
Q

Chemotherapies that are specific to S phase?

A
  • antimetabolites
  • antifolates
  • antipyrimidines
  • antipurines
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4
Q

Chemotherapies that are specific to G1?

A
  • Asparaginase

- Actinomycin D

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5
Q

Chemotherapies that are specific to G0?

A
  • nitrosoureas
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6
Q

Chemotherapies that are specific to mitosis?

A
  • vinca alkaloids
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7
Q

Chemotherapies that are specific to G2?

A
  • bleomycin
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8
Q

Chemotherapies that are phase nonspecific?

A
  • alkylating agents
  • antitumor antibiotics
  • cisplatin
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9
Q

Diff tx modalities for cancer?

A
  • surgery:
    definitive
    staging
    palliative
  • systemic chemo:
    IV vs oral
    neoadjuvant vs adjuvant
  • radiation:
    definitive
    salvage
    palliative
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10
Q

Surgery - diff b/t definitive and palliative?

A
  • surgery may or may not be first step in cancer care (early stage vs mets)
  • definitive:
    tx plan that has been chosen as the best one for the pt after all choices have been considered
  • palliative:
    relieving or soothing the sxs of a disease w/o producing a cure
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11
Q

Diff means of admin of chemo?

A
  • types of cancer tx using drugs to kill the cancer cells
  • admin:
    IV
    injection
    intrperitoneal
    orally
    topically (efudex)
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12
Q

Classes of chemo drugs?

A
  • alkylating agents
  • antimetabolites
  • mitotic inhibitors
  • anthracyclines
  • topoisomerase inhibitors
  • miscellaneous
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13
Q

MOA of alkylating agents? What phase of the cell cycle does it work on? What cancers is it used for?

A
  • one of the first class of drugs discovered of chemo agents
  • MOA: directly damages DNA to keep cell from reproducing
  • works in all phases of cell cycle
  • used to tx: leukemia, lymphoma, hodgkin’s, MM, sarcoma, lung, breast and ovary
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14
Q

Primary toxicities of alkylating agents?

A
  • nausea
  • vomiting
  • myelosuppression
  • alopecia
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15
Q

Classes of alkylating agents?

A
  • nitrogen mustards
  • platinum analogs
  • tiazenes
  • misc.
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16
Q

Types of nitrogen mustards (alkylating agents)? MC one?

A
  • mechlorethamine (nitrogen mustard)
  • ** MC: Cyclophosphamide (cytoxan)
  • Ifosfamide (ifex)
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17
Q

Main SE of Cyclophosphamide (Cytoxan)? What may this lead to? Soln? Other drug that causes this?

A

hemorrhagic cystitis:

  • metabolic products of cytoxan secreted into the urine
  • bladder mucosa may become damaged - may shed large segments of bladder mucosa - lead to prolonged hematuria
  • may lead to urinary obstruction (due to clots)
  • if urine is concentrated may cause severe bladder damage
  • Soln: need to increase fluid intake b/f and after infusion and pee frequently
  • Ifosfamide (Ifex) may also cause this
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18
Q

Types of platinum analogues (alkylating agents)? MC?

A
  • Cisplatin (platinol) **MC
  • Carboplatin (paraplatin)
  • Oxaliplatin (eloxatin)
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19
Q

SEs of Cisplatin (platinol)? What is given to protect against these SEs?

A

nephrotoxicity:
- pts must be vigorously hydrated prior, during and after cisplatin admin
- monitor electrolytes and renal fxn: low K, Na, Mg levels can be seen

neurotoxicity:
- peripheral neuropathy: painful parasthesias
- ototoxicity that can lead to deafness
- Amifostine is given IV to protect against nephro/neurotoxicity from Cisplatin

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20
Q

What long term damage can be caused from alkylating agents?

A
  • Leukemia: b/c these drugs damage DNA they can cause long term damage to bone marrow
  • in rare cases can lead to acute leukemia
  • risk of leukemia is dose-dependent
  • risk of leukemia after getting these agents is highest about 5-10 yrs after tx
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21
Q

MOA of antimetabolites? What phase do these drugs effect? Used to tx what cancers?

A
  • interfere with DNA and RNA growth by substituting for normal building blocks of RNA and DNA
  • Phase: damage cells during S phase when x’somes are being copied
  • tx: breast, ovary, and intestinal tract cancer
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22
Q

Primary antimetabolite toxicities?

A
  • myelosuppression
  • N/V
  • mucositis
  • dermatologic (rash, injection site rxn, dermatitis, pruritus)
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23
Q

Classes of antimetabolites?

A
  • folate antagonists - methotrexate (MTX, trexall)
  • Purine analogs - mercaptopurine (6-MP, Purinethol)
  • pyrimidie analogs: efudex (5-FU), Gemcitabine (Gemzar)
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24
Q

Toxicities of methotrexate? What is given to help ward off toxic effects?

A

(MTX, Trexall)
- MTX toxicity mainly affects cells with rapid turnover:
bone marrow (myelosuppression), mucosa (mucositis)
- can damage liver and kidney
- Sometimes high dose is needed and Leucovorin (reduced folic acid) is given to reverse toxic effects of MTX otherwise pt may die

  • decreased renal clearance: may need prolonged therapy with leucovorin
  • effusions: will go into effusions and leak out continuously and expose normal tissue to drug
  • Vigorous hydration and bicarb loading prevent crystallization of urine in renal tubules
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25
Q

What drugs impair MTX ecretion?

A
  • ASA
  • NSAIDs
  • amiodarone
  • omeprazole
  • PCN
  • phenytoin
  • sulfa compounds
26
Q

MOA of mitotic inhibitors? Work on what phase? Classes?

A
  • plant alkaloids derived from natural products
  • MOA: work by altering DNA inside cancer cells to keep them from growing and multiplying
  • work by stopping mitosis in M phase of cell cycle but can damage all phases by keeping enzymes from making proteins needed for cell reproduction
  • AKA: anti-tumor abx or antimicrotubules
  • classes:
  • vinca alkaloids: Vinblastine, Vincristine (Oncovin)**, Vinorelbine
  • taxanes: paclitaxel (Taxol), docetaxel (taxotere)
  • epothiolone: ixabepilone (Ixempra)
  • anthracyclines
27
Q

Mitotic inhibitors: toxicities and usage in what cancer tx?

A
  • toxicities: myelosuppression, anaphylactic rxns, **peripheral neuropathy
  • used to tx many diff types: breast, lung, myelomas, lymphomas, leukemias
28
Q

MOA and types of Vinca Alkaloids?

A
  • interfere with M phse
  • Vinblastine (Velban)
  • MC: Vincristine (Oncovin)
  • Vinorelbine (Navelbine)
29
Q

SEs of Vincristine (Oncovin)? Most common sx of automonic neuropathy?

A
  • neuropathy: can be caused by all vinca alkaloids but most commonly assoc with Vincristine
  • paresthesias in fingers and toes (mild)
  • sxs can move distal to proximal and result in sig weakness
  • constipation: MC sx of autonomic neuropathy (start on stool softeners at beginning of therapy otherwise may progress to severe stool impaction
30
Q

Class of Anthracyclines?

A
  • Daunorubicin (Cerubidine)
  • Doxorubicine (Adriamycin)
  • Idarubicin
  • Epirubicin
31
Q

SEs of anthracyclines? RFs for this? Most commonly assoc with what anthracycline? How can this be screened for?

A

Cardiotoxicity: leading to systolic CHF - acute (during admin), subacute (days to months following admin), late (yrs following admin)

  • RFs: high cumulative dose (over lifetime), over 70, previous or current chest radiation, cardiac disease
  • MC assoc with doxorubicin ( Adriamycin - MC used anthracycline)
  • Effects may be irreversible
  • Need baseline MUGA scan to calc EF (if greater than 50% proceed, if less than 30% d/c)
  • long term f/u and monitoring for development of CHF/cardiomyopathy is warranted
32
Q

MOA of topoisomerase inhibitors, phase they work in, how are they grouped?

A
  • drugs interfere with topoisomerases, which help separate strands of DNA so they can be copied during S phase
  • Grouped according to which type of enzyme they affect:
    topoisomerase I: Topotecan and Irinotecan (CPT-11)
    topoisomerase II:
    Etoposide (VP-16)
    Teniposide
    Mitoxantrone (also acts as anti-tumor abx)
33
Q

Topoisomerase inhibitors:
tx of what cancers?
Toxiciites?

A
  • tx certain leukemias, as well as lung, ovarian, GI, and other cancers
  • toxicities: myelosuppression, alopecia, GI toxicity
  • Top II inhibitors: can increase the risk of 2nd cancer (AML) - as early as 2-3 yrs after drug is given
34
Q

Misc agents?

A
  • Actinomycin-D
  • Bleomycin
  • Mitomycin -C
  • mitoxantrone (also acts as top II inhibitor)
35
Q

SEs of Bleomycin?

A
  • edema in interphalangeal jts and hardening of skin on palms and soles of feet
  • anaphylactic or serum sickness like rxn
  • **Pulm fibrosis: can be fatal, watch for cough, dyspnea, infiltrates on x-ray
  • Hypotensive rxn:
    severe to fatal after first dose in about 1% of pts
36
Q

Other types of cancer drugs other than chemo?

A
  • targeted therapies
  • differentiating agents
  • hormone therapy
  • immunotherapy
37
Q

What are targeted therapies? MOA? When is it used? Most effective against? Examples?

A
  • newer drugs that attack cancer cells more specifically than traditional chemo drugs
  • most attack cells with mutant versions of certain genes, or cells that express too many copies of a certain gene
  • can be used as part of main tx, or they may be used after tx to keep the cancer under control or keep it from coming back
  • Most effective against: non-hodgkins, leukemia, lung and breast cancer
  • Imatinib (gleevac)
  • Gefitinib (Iressa)
  • Sunitinib (Sutent)
  • Bortezomib (Velcade)
38
Q

MOA and examples of differentiating agents?

A
  • these drugs act on cancer cells to make them mature into normal cells
  • ex:
    retinoids, tretinoin (ATRA or atralin - topical)
    bexarotene (targretin)
    arsenic trioxide (arsenox)
39
Q

Use of hormone therapy? MOA?

A
  • sex hormones
  • change the action or production of female or male hormones
  • used to slow growth of breast, prostate, and endometrial (uterine) cancers, which normally grow in response to natural sex hormones in the body
  • work by making cancer cells unable to use the hormone they need to grow, or by preventing the body from making the hormone
40
Q

Examples of hormone therapy?

A
  • anti-estrogens: fulvestrant, tamoxifen, toremifene
  • aromatase inhibitors: anastrozole, exemestane, letrozole
  • progestins: megesrol acetate
  • estrogens
  • anti-androgens: bicalutamide (casodex), flutamide, nilutamide
  • Gonadotropin releasing hormone (GnRH) aka LHRH agonists or analogs: Leuprolide, and goserelin
41
Q

Diff types of immunotherapy?

Most effective against?

A
  • active: stimulate body’s own immune system to fight the disease
  • passive: doesn’t rely on body to attack disease -
    immune system components (abs) - created outside body and give to fight cancer
    Man made monoclonal ABs designed to attach to cancer cells and mark them for destruction by the immune system - checkpt inhibitors: block signals that cancer cells send out telling immune system not to attack, allows immune system to recognize the tumor
  • immunotherapies most effective against melanoma, kidney cancer, and lung cancer
42
Q

Examples of active immunotherapy?

A
  • monoclonal ab therapy: rituximab (rituxan) and alemtuzumab (campath)
  • non-specific immunotherapies and adjuvants (other substances or cells that boost immune response) - BCG, IL-2, and interferon-alfa
  • immunomodulating drugs - thalidomide and lenalidomide (Revlimid)
43
Q

Chemo cycles?

A
  • chemo given at regular intervals called cycles
  • a cycle may involve a dose of one or more drugs followed by several days or weeks w/o tx:
    this gives normal cells time to recover from drug side effects, sometimes doses may be given a certain number of days in a row or every other day for several days, followed by period of rest, some drugs work best when given continuously over set number of days
  • number of cycles given may be decided b/f tx starts, based on type and stage of cancer
  • in some cases, number is flexible, and will take into account how the tx affects the cancer and person’s overall health
44
Q

Diff chemo regimens?

A
  • adjuvant: set course given to pts with no evidence of disease after surgery or radiation
  • neoadjuvant: aims at eradicating micromet disease or reduce inoperable disease
  • induction: combo chemo given in high dose to cause remission
  • maintenance: also called consolidation, long term, low dose regimen given in remission, maintains remission by inhibiting growth of remaining cancer cells
45
Q

What is radiation therapy?

A
  • ionizing radiation is production of free H+ ions and hydroxyl radicals
  • radiation therapy: use of high energy radiation from x-rays, gamma rays, neutrons, protons, etc. to kill cancer cells and shrink tumors
46
Q

How do you determine dose of radiation therapy?

A
  • tumors have individual radiobiologic characteristics:

unique dose requirements for tx, determined by multiple biologic studies done over time

47
Q

Toxicity of skin radiation?

A
  • erythema: onset 4-14 days
    peak: 4-5 wks
    resolves: 2-6 wks after completion
  • dry desquamation: typicall 5-6 wks, earlier w/ accelerated RT or concurrent chemo, resolves 3-4 wks after completion
  • moist desquamation: following 40-50 Gy, trauma/excess friction, bolus, chemo
    recovery: 2-6 wks after completion
48
Q

Subacute and late toxicities of skin radiation?

A
  • subacute:
    hyperpigmentation:
    as early as 2-3 wks, usually resolves 3-12 mos, occasionally chronic
  • late:
    hypopigmentation in tx field, telangiectasis, fibrosis
49
Q

Toxicity of brain radiation: acute and late?

A
  • acute:
    fatigue, hair loss, erythema of skin, desquamation
  • late:
    cognitive dysfxn, edema, necrosis
50
Q

Toxicity of head/neck radiation: acute and late?

A
  • acute:
    mucositis: odynophagia, dehydration, wt loss
    taste dysfxn
    pain
    xerostomia: may lead to dental caries
  • late:
    permanent xerostomia
    soft tissue fibrosis
    osteoradionecrosis of mandible
    dysphagia
    pharyngeal stricture
51
Q

Toxicity of breast radiation?

A 
- acute: common and temporary
skin redness (90%)
fatigue (70%)
dry desquamation
moist desquamation
pain
- late: uncommon and permanent
fibrosis (15%)
hyperpigmentation (10%)
cosmetic failure (15%)
rib fracture (less than 0.1%)
52
Q

Acute toxicity of lung radiation? Tx of these?

A

esophagitis:

  • mucosal anesthetics (viscous lidocaine)
  • agents that coat the surface (suspension or liquid antacids)
  • liquid analgesics
cough:
- antitussives w/ or w/o codeine
- radiation pneumonitis: bed rest, bronchodilators and corticosteroids
abx not indicated
- skin rxn
- fatigue
53
Q

Late toxicity of lung radiation?

A
  • radiation pneumonitis
  • pulmonary fibrosis (typically not reversible)
  • esophageal stricture
  • brachial plexopathy: superior tumors
54
Q

Acute and late toxicites of esophageal radiation?

A

acute:

  • esophagitis
  • modest skin tanning: posterior
  • fatigue
  • wt loss
  • diarrhea
  • N/V

late:
- esophageal stricure and stenosis (more than 60% of pts)
- perforation:
substernal chest pain, elevated pulse, fever, hemorrhage
- pneumonitis - rare

55
Q

Acute and late toxicities of abdominal radiation of stomach, pancreas and hepatobiliary?

A

acute:

  • dyspepsia: PPI to reduce acid
  • anorexia
  • nausea: prophylactic zofran prior to tx
  • fatigue

late:

  • bowel obstruction
  • worsening diabetes 2nd to worsening pancreatic fxn
  • liver/kidney: usually kept at safe doses, renal failure, HTN
56
Q

Acute and late toxicities of pelvic radiation?

A 
acute:
- diarrhea - common: imodium, lomotil
- rectal irritation: rare (pain and bleeding)
- urinary sx:
freq/urgency
dysuria
nocturia
retention
- fatigue
late:
- persistent urinary sx:
frequency, nocturia, incontinence
- bowel changes: loose stools
- erectile dysfxn
57
Q

Acute and late toxicities of anal radiation?

A 
acute:
- skin rxns:
dry and/or moist desquamation
- leukopenia
- thrombocytopenia
- proctitis
- diarrhea
- cystitis

subacute/late:

  • chronic diarrhea
  • rectal urgency
  • sterility
  • impotence
  • vaginal dryness
  • vaginal fibrosis
  • possible decreased testosterone
58
Q

Toxicities of GYN radiation? tx?

A
  • cystitis
  • proctitis
  • fistula: rectovaginal, vesicovaginal
  • vaginal ulceration/necrosis
  • vaginal stenosis
  • skin rxns (rectal, anal, vulvar):
    desquamation: tx with hydration, domeboro soaks, silvadene, and narcotic pain meds
    attempt to decrease dose to external genitalia to reduce skin rxns (groin and interglutteal clefts)
59
Q

What is the only systemic side effect of radiation?

A
  • fatigue
60
Q

Degree of damage is dependent on what tx regimen related factors?

A
  • types of radiation used
  • total dose admin
  • field size/fractionation
61
Q

Late side effects caused by radiation should be a dx of what?

A
  • dx of exclusion
  • explore other causes of sxs
  • discuss with radiation oncologist who can look at the plan to verify radiation as cause

Oncology (11 decks)

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