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Oncology Flashcards

1
Q

what are the 5 broad cancer therapy categories?

A
  • cytotoxic
  • anti-hormonal
  • targeted
  • immunotherapy
  • blood and marrow transplant
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2
Q

what are 4 characterstics of cancer cells ?

A
  • Uncontrolled cellular growth
  • Ability to invade adjacent structures and travel to distant areas
  • Incapable of physiologic functions of the mature tissue of origin
  • Altered proteins enzymes and cytogenetics
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3
Q
  1. How are tumors staged?
  2. Ajuvant chemotherapy means?
  3. Neoadjuvant chemotherapy means?
A
  1. TNM staging - (Tumor, Nodal Status, Metastasis ) for solid tumors (Stage I, II, III, IV)
  2. Given after surgery to reduce risk of local and systemic occurence
  3. Given prior to surgical intervention to reduce tumor size to remove micrometastases
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4
Q

Cytotoxic chemotherapy is ?

A

toxic to all cells but more specific to rapidly dviding cells

→Thats why you get the N/V because it attacks the GI tract mucosa

→Thats why you lose hair because it attacks the hair follicles

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5
Q
  1. What does doubling time mean ?
  2. What is Gompertzian growth?
  3. What is log-kill hypothesis
A
  1. Time needed for a tumor cell population to double in size
  2. Early growht is exponential, but as tumor gets bigger, growth slows due to decreased nutrients/blood supply
  3. A given dose of chemotherapy kills the same fraction of tumor cells regardless of the size of the tumor at the time of treatment
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6
Q
  1. Dosing of cytotoxic chemotherapy is based off of ?
  2. Cytotoxic chemo is administered in ____ every…..?
A
  1. dosing is based off of body surface area and actual weight
  2. Cytotoxic chemo is administered in cycles every 14, 21, or 28 days
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7
Q

Dose Intensity vs. Dose Density

A
  • Dose Intensity
    • More chemo in a shorter period of time
  • Dose Density
    • The amount of chemo you are getting in a set period of time
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8
Q

1012 cancer cells =?

100 cancer cells =?

A
  • death
  • want to shrink tumor to this # otherwise they will regrow
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9
Q

Alkylating Agents

  1. MOA?
  2. Specific to?
  3. Alkylating Agents Toxicities ?
A
  1. Prevents cell division by cross-linking DNA strands and decreasing DNA synthesis (doesn’t allow DNA strands to unzip which they need to in order to replicate)
  2. Cell cycle non-specfic

3.)

  • N/V (mostly acute-some delayed)
  • Myelosupression -dose limiting factor
  • Alopecia
  • Infertility
  • Secondary Malignancies
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10
Q

Specific Alkylating Agents and Their Toxicities

A
  • Cyclophosphamide/Isofamide
    • Hemorrhagic cystitis (primarily ifosfamide) due to acrolein metabolite
      • Use Mensa to prevent bleeding in the bladder (hemorrhagic cystitis)
  • Cisplatin
    • Nephrotoxicity
    • N/V (acute and delayed)
    • Ototoxicity
  • Oxaliplatin
    • Neuropathies
      • made worse by cold tempatures
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11
Q
  1. What are antimetabolites ?
  2. What is their MOA?
A
  1. Structural analongs of naturally occuring substances necessary for specific biochemical rxn’s -mimic purine and pyrimidines
  2. A.) compete with normal metabolities B.) fasely insert themselves for a metabolites normall incorporated into DNA and RNA
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12
Q
  1. What are the comon toxicities of Antimetabolities ?
  2. What are the drug specific toxicities of antimetabolities (can occur at high doses)?
A

1.)

  • Myelosupression
  • Mucositis
  • Mild N/V/D

2.)

  • Methotrexate
    • renal toxicity
      • given very high dose of methotrexate and then give Leucovorin as rescue dose
  • Cytarabine
    • Cerebellar toxicity
  • Flurouracil
    • Leucovorin propentiates this medication
  • Capecitabine
    • Hand-foot syndrome
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13
Q

Can you give methotrexate and cisplatin together?

A

NO - both are renally toxic don’t give together

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14
Q

What Natural Cancer products do we have available? (4 things)

A
  1. Antitumor antibiotics
  2. Plant alkaloids-vinva alkaloids, taxanes, topoisomerase I & II
  3. Marine-based products
  4. Enzymes
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15
Q

Antracyclines

  • Class?
  • MOA?
  • What toxicity can they cause?
  • How much can you give of this class?
A
  • Antitumor antibiotics
  • MOA: block DNA and RNA transcription
  • Congestive heart failure-cardiac toxicity
  • There is a life time max dose
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16
Q

Bleomycin

  1. Class?
  2. Toxicity that it can cause
  3. How much can you give of this dose?
A
  1. Antitumor antibiotics
  2. Pulmonary fibrosis
  3. There is a lifetime max dose
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17
Q
  1. The myocardiotoxicity of antitumor antibiotics is directly related to ?
  2. MOA?
  3. Early toxicity?
  4. Late toxicity ?
A
  1. Dose dependent
  2. Production of toxic free radicals -membrane lipid peroxidation leading to irreversible damage and replacement by fibrous tissues
  3. Early- HF can develop w/n 3 months
  4. Late-symptoms can appear one decade following completion
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18
Q

Dexrazoxane

  • Purpose?
  • MOA?
A
  • decreases risk of cardiotoxicity w/ anthracyclines
  • MOA: EDTA-like chelating agent
    • binds intracellular iron released following lipid peroxidation
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19
Q

Doxorubcin

  1. Class?
  2. Toxicity that can come from it?
  3. What must you do before administering this drug to a patient?
A
  1. Anthracyclines
  2. Cardiac toxicity
  3. Must have cardiac function assessed before given dose
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20
Q

MOA and Classes of Mitomycin and Dactinomycin?

A

Mitomycin

Class: Antitumor antibiotics

MOA: Cross-links DNA

Dactinomycin:

Class: Antitumor antibiotics

MOA: Blocks RNA synthesis

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21
Q

Microtubule Agents

  1. Class?
  2. MOA?
  3. Subcategories?
A

Class: Natural products (cancer)

*Different MOAs –> All work in M phase
“Anti-mitotics”

*Synthetic and semi-synthetic

*Works in M phase of cell cycle

  • Vinca alkaloids
  • Taxanes
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22
Q

Anti-mitotics cause….

A

PERIPHERAL NEUROPATHY

23
Q

Docetaxel

  1. Class?
  2. Toxicities?
A

Class: Taxanes (microtubule agent)

ADR:

  • **Neuropathies**
  • Peripheral edema
  • Hypersensitivity reactions
24
Q

Paclitaxel

  1. Class
  2. Toxicities?
  3. How can you prevent the toxicities?
A

Class: Taxanes (microtubule agent)

ADR:
- **Hypersensitivity
reactions
- Neuropathies

**PRE-MEDICATE:

  • H1 and H2 blocker
  • Steroid
25
Q

Taxanes and Vinca alakoids

  1. Class?
  2. They are considered?
A
  1. Microtubule agents
  2. Anti-mitotic
26
Q

Vinorelbine and Vinorelbine

  1. Class?
  2. ADR?
A

Class: Vinca alkaloid (microtubule agent)

ADR:
- Myelosuppression (only Vinorelbine)

27
Q

Vincristine

  • Class?
  • ADR?
A
  • Class: Vinca alkaloid
  • ADRs:
    • Neuropathy
    • Constipation
    • Do not give intrathecally- causes death
28
Q

Topoisomerase I inhibitors

  • Class?
  • MOA?
A
  • Class- plant alkaloid (natural product)
  • MOA- Inhibits enzyme that is trying to repair DNA of cancer cell
29
Q

Topoisomerase II inhibitors

  • Class?
  • MOA?
A
  • Class: alkaloids (natural product)
  • MOA: inhibit enzyme that is trying to repair DNA of cancer cell
30
Q

Topoisomerase inhibitors cause…..

31
Q

Irinotecan

  • Class?
  • ADR?
    • how is it treated?
A
  • Class- topoisomerase I inhibitor
  • ADR-diarhea (i ran to the can)
    • Immediate-cholinergic rxn
    • delayed -give loperamide or anticholinergic
32
Q

Etoposide

  • Class?
  • ADR?
A

Class: Topoisomerase II inhibitors

ADR:
- Secondary cancers

33
Q

Asparaginase

  • class?
  • ADR?
A
  • Class-natural product (enzyme)
    • taken up by cancer cells and kills cancer cells because cancer cells can’t make this product
  • ADR-hypersensitivity rxn
34
Q

Marine-based Products

  • Class?
A

Class: Natural cancer product

35
Q

Eribulin

  • Class?
  • Toxicities?

Trabectedin

  • Class?
  • Mechanism?
  • ADR?
A

Eribulin

  • Class-marine based product
  • Toxicities-peripheral neuropathy and CINV

Trabectedin

  • class-marine based product
  • mechanism -somewhat like alkylating agent
  • ADR-hand-foot syndrome and CINV
36
Q
  1. What is the MOA of hormonal treatment?
  2. Anti estrogen therapy is for ?
  3. Anti androgen therapy is for?
  4. Lutenizing hormone-releasing hormone (LHRH) therapy is for?
A
  1. blocks production of hormones or hormone receptors in body
  2. breast cancer
  3. prostate cancer
  4. shuts down production of hormones
37
Q

Tamoxifen

  • Class?
  • MOA?
  • Indication ?
  • Benefit?
  • ADR?
A

Class: Selective estrogen receptor modulator (Hormone therapy)

*Antagonist –> Blocks estrogen receptors

**Use: For Premenopausal, postmenopausal women that are trying to decrease the odds of their breast cancer recurrence

Benefits: Increases 15 year survival by 31%

ADR: Increase risk of endometrial cancer

38
Q

Letrozole, Anastrozole, Exemestane

  • Class?
  • Indication?
  • ADR?
A
  • Aromatase inhibitor
  • Decrease the recurrence of breast cancer in postmenopausal women
  • ADR: osteoporosis/fracture
39
Q

LHRH agonist

  • MOA?
  • ADR?
A
  • Inhibits pituitary through negative feedback from releaseing LH and FSH
    • stops testes from producing testosterone (prostate cancer) can also stop ovaries from releasing estrogen (breast cancer)
  • Tumor flare
    • can occur in first week but then fixes itself
40
Q

Leuprolide

Class?

Use?

A

Class: LHRH agonists

  • Prostate cancer
41
Q

Goserelin

  • Class?
  • Use?
A

Class: LHRH agonists

  • Prostate cancer
42
Q

Triptorelin

  • Class?
  • Use?
A

Class: LHRH agonists

  • Prostate cancer
43
Q

Degarelix

  • Class?
  • MOA?
A
  • Class- LHRH ANTagonist
  • MOA-Directly inhibits pituitary from releasing LH and FSH
44
Q

Bicalutamide

  • Class?
  • MOA?
A
  • Class-antiandrogen
  • MOA-blocks androgen receptor
45
Q

What are the 2 purposes of target agents?

A
  1. Identify certain features of a cancer cell that make it different from normal cell
  2. Prevent tumors cells from entering cycle that trigger growth, metastasis, and immortality
46
Q

Monoclonal antibodies Vs. Molecularly target therapies?

  • Class?
  • Purpose?
  • Drugs available?
A
  • Mono: antibodies that match an antigen on cancer cell surface
    • drugs end in “mab”
  • Molecular: block signaling inside cell
    • drugs end in “nib”

** both are class: targeted agents

47
Q

VEGF signaling pathway (VSP) inhibitors vs EGFR inhibitors

  • What are they?
  • ADR?
A
  • VEGF inhibitors
    • vascular endothelial growth factors receptor inhibitor
      • HTN
      • BLEEDING
  • EGFR inhibitors
    • epidermal growth factor receptor inhibitor
      • Acneiform rash-may indicate effectiveness
        • treat with tetracycline
48
Q

mTOR inhibitors

  • What is it ?
  • ADR’s?
  • DDI?
A
  • mammalin target of rapamycin (mTOR)
  • ULCERS** and hyperglycemia
  • 3A4 DDI’s
49
Q

BCR-ABL mutation inhibition

  • ADR
    • treatment?
A
  • N/V (low level constant nausea)
    • dexamethasone
50
Q

Do target therapies cure cancer?

A

No, they just make it a chronic disease

51
Q

CD20 target: uses &causes?

A
  • ADR: infusion rxn
  • targets B cells (lymphoma)
52
Q

HER2 inhibition cuases ?

What cant you give this with?

A
  • Hand-foot syndrome (Lapatinib)
  • CARDIOTOXICITY
  • Cant give with antrhacycline (too much toxicity)
    • trastumab (HER2 inhibitor)
      anthracyclines (doxorubicin)
      • THIS IS A NO NO COMBINATION
53
Q

Targeted therapy ADRs?

Target therapy causes?

A
  • Hair depigmentation
  • Dysphonia
  • Hypothyroidism
  • CAUSES fatigue
54
Q

Small molecule inhibitors (molecularly target therapies) might cause ?

A
  • These are the drugs that end in mab
  • might cause QTc prolongation

Pharm II (12 decks)

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