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Year 3 - Clinical (Winter) > 28 - Oncology 2 > Flashcards

28 - Oncology 2 Flashcards

1
Q

Define adjuvant therapy

A

Systemically administered therapy w/ cytotoxic drugs, hormones, or biologic response modifiers to kill micrometastases after the primary tumour has been eliminated (ex: chemotherapy after surgery to remove the tumour)

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2
Q

Define neo-adjuvant therapy

A

Tx given before surgery to reduce tumour and allow better surgical resection

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3
Q

Define remission

A
  • Complete disappearance of cancer sx, typically occurring when the number of cancer cells decrease below 109
  • Complete remission isn’t the same as being cured
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4
Q

Define 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

Factors that determine tx modality

A
  • Cancer type
  • Location and size of tumour
  • Extent of disease
  • Radiosensitivity or chemosensitivity
  • Hx of prior therapy
  • Concurrent organ dysfunction
  • Performance status (overall physical functioning)
  • Px goals/wishes
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6
Q

Cancer tx modalities

A
  • Surgery
  • Radiation therapy
  • Chemotherapy
  • Biological and targeted therapy
  • Immune therapy
  • Supportive care
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7
Q

Describe surgery as a cancer tx

A
  • Essential for diagnosis of cancer and for staging of many solid tumours
  • Some of the role’s surgery can play in cancer management:
    • Curative tx for localized mass
    • Reduce size of the tumour
    • Remove isolated metastatic disease
    • Treat complications (ex: obstruction, hemorrhage, or perforation)
    • Reconstruct anatomic defects to improve function or appearance
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8
Q

Describe radiation therapy as a cancer tx

A
  • Breaks bonds in DNA causing loss of proliferative capacity
  • Induces apoptosis
  • Plan to deliver tumoricidal dose w/in limits of tolerance of surrounding normal tissues
    • Normal tissues are usually able to recover better than cancer cells
  • Methods of delivery:
    • External beam (teletherapy)
    • Internal (brachytherapy) -> high dose rate w/ remote leading, or low dose rate implanted (temporary or permanent, ex: prostate seeds)
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9
Q

Common radiation SE

A
  • General = radiodermatitis, fatigue, weight loss due to anorexia
  • Site-specific
    • Myelosuppression (skull, sternum, long bones)
    • Radiation pneumonitis/ pulmonary fibrosis
    • Reproductive system
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10
Q

Basic skin care highlights for post-radiation

A
  • Bathing is OK unless open areas; no scrubbing of skin, pay dry
  • Deodorants and antiperspirants OK unless skin reaction
  • No talc, baby powder, or cornstarch in tx area
  • No tape, perfume, alcohol, or jewelry in tx area
  • Avoid ice packs or heating pads
  • No tanning lamps, petroleum products, or shaving
  • Don’t apply moisturizers w/in 2 h of tx
  • Avoid sun on tx area
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11
Q

What is chemotherapy? Goal?

A
  • The use of cytotoxic medications to kill cancer cells
  • Goal = reduce and/or eliminate visible and invisible (micrometastases) disease
  • Cancer cells can develop resistance to chemotherapy
  • Most often is systemic, therefore produces systemic SE
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12
Q

Principles of chemotherapy

A
  • Start therapy when tumour burden is low and growth fraction is high
  • Use a combination of drugs
  • Use a dosing schedule that limits tumour regrowth during host tissue recovery
  • Dose to maximum tumour response or toxicity before changing therapy
  • Therapeutic benefit must exceed toxicity
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13
Q

Chemotherapy routes of administration

A
  • Oral – increasingly common
  • IV – bolus over mins/hrs and/or CIVI over days
  • Intra-thecal – b/c most chemo doesn’t cross BBB
  • *Only certain drugs are ok via this route; all other drugs are fatal
  • IM – L-asparaginase
  • Intra-cavitary – ex: bladder
  • SC – may be used for basal cell skin cancer
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14
Q

Principles of combination chemotherapy regimens

A
  • Drugs are active against the tumour when used alone
  • Drugs that have a biochemical basis for suspected synergy
  • Drugs that have different mechanisms of action
  • Drugs that produce toxicity in different organ system (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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15
Q

Chemotherapy tx plan

A
  • Most often given in combination according to specific research-based protocols
  • Combos are usually identified by acronyms:
    • R-CHOP (rituximab, cyclophosphamide, hydroxydaunorubicin, oncovin, prednisone)
    • ESHAP, FEC, FolFOX
  • Px are often part of clinical trials
  • Doses carefully calculated according to body surface area
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16
Q

Classification of chemotherapy agents

A
  • Alkylating agents
  • Antimicrotubule agents
  • Antimetabolites
  • Antitumour antibiotics
  • Nitrosureas
  • Corticosteroids
  • Hormones
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17
Q

Alkylating agents – how do they work? Cell cycle specific or non-specific?

A
  • Contain highly reactive ions on their chemical structure
  • In some cases, must be activated/ converted in the body to create the highly reactive, positively charged ions
  • These positively charged ions react w/ electron-rich portions of the cell (proteins & DNA) to form strong chemical bonds thus leading to inhibition of DNA synthesis
  • Cell cycle non-specific
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18
Q

Cisplatin – toxicity, role

A
  • Dose limiting toxicity = nephrotoxicity
  • One of the most emetogenic antineoplastics
    • Can display delayed N/V
  • Other toxicities = myelosuppression, neuropathy, alopecia, and permanent ototoxicity
  • Has a role as radiation sensitizer
  • Very important agent used for the tx of testicular cancer, lung cancer, head and neck, breast cancer
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19
Q

What is the main difference between carboplatin and cisplatin?

A

Carboplatin has more toxicities than cisplatin; main toxicity is to platelets

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20
Q

Antimicrotubule agents – MOA and cell cycle specific or non-specific?

A
  • Usually block a particular enzyme, or arrest the cell in some step of mitosis or cell division
  • Cell-cycle specific
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21
Q

Plant alkaloids – vincristine (cell cycle specificity, toxicity)

A
  • Vinca alkaloid
  • Cell-cycle specific inhibition of microtubule formation
  • Dose limiting toxicity = peripheral neuropathy
    • Other toxicities = constipation, extravasation
  • Inadvertent intrathecal administration is usually fatal
22
Q

Antimetabolites – MOA, subgroups, cell cycle specificity

A
  • Act by interfering w/ the metabolic processes of the cell
    • Interfere w/ nucleic acid biosynthesis
  • Subdivided into folate antagonists, purine analogues, and pyrimidine 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
23
Q

Fluorouracil – MOA, role

A
  • Most extensively studied and used agent in colorectal cancer
    • Interferes w/ RNA synthesis and function
    • Blocks the enzyme, thymidylate synthase
  • Pattern of fluorouracil toxicity differs between bolus administration and continuous infusion
  • Useful as a radiation sensitizer
24
Q

Antitumour antibiotics

A
  • Act by binding to or complexing w/ DNA and/or RNA, thus inhibiting replication
  • 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
25
Q

Doxorubicin (antitumour antibiotic) – use, AE

A
  • Anthracycline antibiotic w/ a lifetime cumulative dosage (500-550 mg/m2)
  • Most serious dose limiting SE = cardiomyopathy
  • Extensive use for tx of breast cancer and lymphomas
  • Can produce radiation recall (develop a rash in the place they previously had radiation)
26
Q

Bleomycin (antitumour antibiotic)

A
  • Damage DNA and prevent repair
  • Dose-limiting toxicity = pulmonary fibrosis
  • Active agent for tx of lymphomas, testicular cancer
  • Development of chills/fever post-tx
  • Cell cycle specific
27
Q

What is tumour lysis syndrome?

A
  • Tumour cells undergoing cancer therapy release phosphates, calcium, potassium, nucleic acids, and lactates
  • This results in hyperphosphatemia/ hypocalcaemia, hyperkalemia, hyperuricemia, and acidosis
    • This can result in acute kidney injury
  • More common in some tumours; depends on how large tumours are and how spread out they are
    • A concern in those w/ lymphomas or leukemias
  • Sometimes choose chemotherapy that is milder or radiation to shrink the tumour then do the primary chemotherapy to lessen this syndrome
    • Can also use allopurinol for prevention
28
Q

Chemotherapy – acute reactions

A
  • Vomiting -> prevent w/ anti-emetics

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

29
Q

Chemotherapy – delayed effects

A
  • N/V (especially w/ cisplatin; causes both acute and delayed N/V)
  • Mucositis of varying severity, diarrhea
  • Alopecia
  • Bone marrow suppression; bleeding due to decreased platelets
  • Fatigue due to decreased Hgb and other factors
  • Skin changes -> dryness, flaking, peeling
30
Q

Major chemotherapy factors predicting risk for acute chemotherapy induced N/V

A
  • Intrinsic emetogenicity of chemotherapeutic agent
  • Dose, route of administration
  • Rate of infusion
  • Repeated cycles of chemotherapy
31
Q

Major pt factors predicting risk for acute chemotherapy induced N/V

A
  • Pt characteristics (low alcohol consumption, < 50 y/o, female, hx of motion sicknes)
  • Poor control w/ prior chemotherapy
32
Q

Major chemotherapy factors predicting risk for delayed chemotherapy induced N/V

A

Not well characterized in many chemotherapeutic agents

33
Q

Major pt factors predicting risk for delayed chemotherapy induced N/V

A
  • Pt characteristics (low alcohol consumption, < 50 y/o, female, hx of motion sicknes)
  • Poor control of acute chemotherapy induced N/V (**most important factor)
34
Q

Which drugs can be used as anti-nauseants?

A
  • Steroids (dexamethasone)
  • Serotonin antagonists (ondansetron)
  • Dopamine receptor agents (haloperidol, domperidone, metoclopramide)
  • BZDs (lorazepam) -> used for px w/ anticipatory N/V
  • Neurokinin-1 blockers (aprepitant)
  • Cannabinoids (nabilone, dronabinol)
35
Q

Effects of bleomycin, doxorubicin, mitoxantrone, MTX

A

Mucositis

36
Q

Effects of cytarabine, 5-FU

A

Mucositis, diarrhea

37
Q

Effects of high dose melphalan

A

Esophagitis, stomatitis, diarrhea, colitis

38
Q

Effects of high dose etoposide

A

Oropharyngeal mucositis

39
Q

Hematopoeitic therapy

A
  • Granulocyte colony-stimulating factor (GCSF)
    • Stimulates production, maturation, regulation, and 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
    • Supportive care, not cancer tx
  • Erythropoeitin -> used more commonly w/ renal disease than cancer
  • Transfusions of RBCs and platelets are used instead of growth factors
40
Q

Cardiac toxicity w/ antineoplastics

A
  • Known dose limiting toxicity of several agents
  • Common w/ anthracycline antibiotics (ex: doxorubicin, epirubicin, daunorubicin, idarubucin, mitoxantrone)
  • Seen w/ some of the MAbs
  • Risk factors for cardiac damage = age, pre-existing heart disease, concurrent tx w/ cyclophosphamide, tx schedule
41
Q

Peripheral neurotoxicity w/ 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
42
Q

Pulmonary toxicity w/ antineoplastics

A
  • Rare but often fatal complication of cancer chemotherapy
  • Usually a result of inflammation and subsequence formation of scars in the lungs after administration of certain chemo drugs
  • Sometimes referred to as pneumonitis or pulmonary fibrosis
  • Dose limiting toxicity of agents such as bleomycin, busufan, carmustine
  • Concern if pt is to receive chest irradiation
43
Q

Late effects of chemotherapy

A
  • Risk for leukemias and other secondary malignancies
    • Radiation and chemotherapy can induce DNA damage that can lead to new malignancies other than original disease
  • Secondary malignancies other than leukemia also possible
    • Includes breast (especially women who had chest radiation w/o shielding prior to 1980’s), uterine, thyroid, lung
    • Secondary malignancies usually tx resistant
44
Q

What is “targeted tx” for cancer? What are some examples?

A
  • “Drugs or substances that block the growth and spread of cancer by interfering w/ specific molecules involved in tumour growth and progression”
  • Tyrosine kinase inhibitors -> imatinib (chronic myelogenous leukemia/CML), erlotinib (NSCLC), dasatinib and nilotinib (CML)
45
Q

Biological tx for cancer; what is it and which products are approved

A
  • “Uses living organisms, substances derived from living organisms, or synthetic version of such substances to treat cancer”
  • Approved = MAb, cytokines
46
Q

Describe the steps to produce a protein (for a MAb)

A
  1. Gene from a desired protein is combined w/ a DNA sequence
  2. Recombinant DNA sequence is inserted into a host cell
  3. Host cell is grown in culture to reproduce the desired protein
47
Q

Describe biosimilars

A
  • Impossible to produce a “generic” of a biologic b/c must have the exact same manufacturing process to be considered the same
  • Enter the market subsequence to an innovator version previously authorized in Canada
  • Have demonstrated similarity to the reference biologic
  • Are highly similar but not identical; any difference in product attributes should have no adverse impact on safety and efficacy
  • Biosimilars don’t have to go through phase 3 trials
48
Q

Monoclonal antibodies for cancer

A
  • Engineered to bind to specific targets on cell surface
  • Rituximab -> targets CD20 on surface of normal & cancer cells
  • Zevalin -> also targets CD20; has a radio isotope attached to the MAb that gives off radiation when it binds to the cell (normal and cancer); so better killing of cancer cells, but more toxicity; used for px who don’t respond well to rituximab
  • Bevacizumab -> MAb that targets VEGF receptor and inhibits angiogenesis
49
Q

Role of cytotoxic T-cells in cancer

A
  • T-cells are a type of lymphocyte that play an active role in the immune response
  • T-cells recognize and eliminate foreign or abnormal cells, including cancer cells
  • Cancer cells are smart and also have mechanisms to evade T-cell recognition
50
Q

What are BITEs? What is an example?

A
  • Bispecific T-cell engager (BiTE) Ab w/ dual specificity for CD19 and CD3
  • Simultaneously binds CD3 positive cytotoxic T cells and CD19-positive B cells, resulting in T-cell mediated lysis of normal and malignant B-cells
  • Engages px endogenous T cells to attack and eradicate B-precursor leukemic blasts
  • Blinatumomab
51
Q

What do PD-1/ PD-L1 inhibitors do?

A
  • PD-L1 ligand is present on normal tissue, causes T-cell not to target normal tissues
  • Some tumours have developed the ability to overexpress the PD-L1 ligand, so it tricks the T-cell to believe it’s a normal host cell and won’t kill it
  • Good for px that are resistant to all other chemotherapy drugs (considered a “salvage” therapy)
52
Q

Bicalutamide – MOA, role, and SE

A
  • Useful for tx of prostate cancer
  • Inhibit translocation of androgen receptor not allowing testosterone to bind
  • Useful in combo w/ gonadotropin-releasing hormone analogues
  • Oral medication; major SE = diarrhea

Year 3 - Clinical (Winter) (30 decks)

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