Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm III, Exam 3 Need to Knows > Oncology Need to Knows > Flashcards

Oncology Need to Knows Flashcards

1
Q

Define Solid Tumors

A

Affect organ & other solid tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define Hematologic Malignancies

A

affect blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define primary tumor

A

original mass of cancer cells of a solid tumor in a body organ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define Metastasize

A

spread of cancer from the primary tumor to body sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

4 modalities used in the treatment of cancer

A
  • surgery
  • radiation
  • chemo
  • immunomodulation (stem cell transplant, immunosuppressive or immunostimulatory agents (systemic therapies))
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain how the principal of log cell kill kinetics is applied in the use of chemotherapy?

A
  • a given tx kills a constant fraction of cells
  • Subsequent doses reduce the cancer burden proportionally over time
  • More cells killed, the higher the chance for cure.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the principle of cancer cell growth that describes how the growth fraction of a tumor changes over time?

A

Gompertzian model of tumor cell growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Gompertzian model of tumor cell growth

A
  • Growth fraction of a tumor is not constant
  • Growth factor decreases as the tumor gets larger
  • Results in decreased number of cells susceptible to chemo.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain why multiple chemotherapy drugs are typically combined into one treatment regimen? What other factors besides mechanism of action are considered when designing chemotherapy combinations?

A
  • Efficacy: each drug in a regimen must has some anticancer activity when used alone
  • Toxicity: Select drugs to minimize overlapping toxicities
  • Optimum scheduling: each drug should be given in intervals (daily, weekly, monthly, etc) to max activity
  • Mechanism of action: multiple mechanisms of action help overwhelm cells ability to develop resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is dose density and how could it change while a patient is being treated with chemotherapy?

A
  • Giving repeated doses of multiple chemotherapy agents over a period of time.
  • →Chemotherapy cycles (give same drugs once every 1-4 weeks)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Neoadjuvant chemotherapy

A

Used prior to the use of local therapies to improve their effect by reducing the size of the tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Adjuvant chemotherapy

A

Used after local therapies to improve their long term effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cure

A

sustained cancer-free period, a prolonged period of remission (usually 5 years)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Control

A
  • reduce cancer burden, prevent extension of cancer, and extend survival
  • cure is unlikely
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Palliation

A
  • reduce symptoms of disease, improve quality of life, and prolong survival
  • cure is not likely
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Remission/complete response

A

unable to detect presence of cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

partial response

A

reduction in tumor burden but cancer is still present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Treatment failure/progressive disease

A

cancer continues to grow despite treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe 3 possible mechanisms why chemotherapy might not work in a patient

A
  • Mutations within cancer cells could: – Block chemotherapy actions, – Block uptake of chemo into cells, Facilitate excessive transport of drug back out of the cells
  • Drug interactions could decrease exposure to chemo within the patient’s body: Increased metabolism of chemo agents ↓ body concentrations
  • Calculated dose did not match patients’ individual body characteristics. Metabolic rate, distribution of the drug throughout the body to site of cancer.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is salvage chemotherapy and when it’s used?

A
  • Use of other combo of chemo drugs

- used when primary tx unsuccessful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe the difference between cell cycle specific and cell cycle nonspecific Agents
Cell cycle impact:

A

based on whether the agent requires to be in active phases of the cell cycle (g1, s, g2, m) or can be in resting phase (g0) as well as other phases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

MOA of Cyclophosphamide

A

Disrupts normal DNA structure by altering atomic interactions and prevents use of DNA as a blueprint for cell division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

MOA of Cisplatin

A

Acts similar to alkylating agents by binding DNA and forming intra- and interstrand crosslinks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

MOA of MTX

A

-Inhibits DHFR which converts one form of folic acid to another (blocks purine synthesis)
-also inhibits TS = blocks incorporation of FUTP into RNA and dFUTP into DNA blocking formation of RNA and DNA
-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

MOA of Vincristine

A
  • Inhibit tubulin polymerization required for microtubule assembly
  • Prevents microtubule formation
  • Microtubule inhibition blocks cell division during metaphase and causes cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

MOA of Paclitaxel

A

Act by promoting microtubule formation

  • prevent spindle fibers from retracting
  • Preventing disassembly of microtubules blocks completion of cell division and leads to cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

MOA of Etoposide

A
  • Act by inhibiting DNA topoisomerase II

- Prevents proper unwinding of DNA resulting in blockade of DNA synthesis and cell division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

MOA of Doxorubicin

A
  • Inhibit topoisomerase 2
  • Bind to DNA and intercalate DNA strands
  • Generate free radicals
  • Bind to cell membranes and alter fluid and ion transport
  • DNA intercalation: drug binds to areas on both strands preventing DNA from being replicated
  • Free radical formation: free radicals are very damaging to tissues by binding to metabolic products and disrupting cellular functions
29
Q

MOA of Imatinib

A

-Tyrosine kinases are families of proteins that use ATP to
phosphorylate other proteins
-Often exist as receptors on the surface of cells waiting to receive a signal to do what they do best
-Phosphorylation of other proteins by TK is used to regulate cell growth functions
-Tyrosine kinases are often over-active in cancer cells leading to enhanced tumor growth activities

30
Q

MOA of Thalidomide

A
  • Unclear
  • May alter tumor necrosis factor (TNF) levels
  • May increase activity of NK cells, IL-2, and interferons
  • May promote apoptosis
31
Q

MOA of Bortezomib

A
  • Inhibit complexes of proteins that would otherwise break down unneeded or damaged proteins
  • Promote activation of signaling pathways that trigger apoptosis
32
Q

MOA of Trastuzumab

A
  • Specially designed antibodies made using biotechnology
  • Target specific proteins in cancer cells and block their standard function
  • Usually bind to various sites on receptors such as EGFR, HER2, or CD antigens
33
Q

MOA of Asparaginase

A
  • Enzyme antineoplastic agent
  • Breaks down asparagine to aspartate
  • Many tumor cells are unable to make asparagine (but normal cells can)
  • breaks down available asparagine and deprives tumor cells of the necessary amino acid
  • Leads to cell stress and apoptosis
34
Q

Explain the 4 possible mechanisms that monoclonal antibodies use to kill tumor cells.

A
  • Could block receptors required for activating cell functions
  • Could bind to free protein ligands looking to bind to receptors
  • Could bind to receptors and trigger apoptosis
  • Could bind to receptors and trigger antibody dependent cellular cytotoxicity (ADCC)
35
Q

Describe the purpose of using leucovorin when used with either fluorouracil or methotrexate

A
  • Reduces methotrexate toxicity by rescuing normal cells
  • Bypasses inhibition of DHFR by MTX
  • ↑ 5-FU activity against colon CA = Enhances binding of 5-FU to TS
36
Q

What is the process of cancer cell death that results from the action of tyrosine kinase inhibitors?

A
  • TKIs can target, bind to, and block specific sites on various tyrosine kinases
  • The sites are needed to activate the tyrosine kinase
  • Results in inhibiting specific regulatory pathways and promotes cancer cell death through apoptosis
37
Q

What is the mechanism by which resistance to TKIs may occur?

A

Mutations in the amino acid sequence of the tyrosine kinase could prevent the TKI from binding to the targeted site and make the drug ineffective

38
Q

What are two mechanisms of drug interactions with TKIs?

A

-Many are metabolized by CYP450 enzyme system
Ex: CYP3A4

-Enzyme inhibitors (azoles) can ↓ metabolism and ↑ risk for side effects

•-Enzyme inducers (phenytoin) can ↑ metabolism and ↓ effectiveness

•-Reduced bioavailability w/PPIs and H2 antagonists can ↓ effectiveness

39
Q

Define Vesicant

A

tending to cause a blister

40
Q

Define Extravasation

A

leakage of fluid out of its container

41
Q

List 2 families of drugs w/vesicant activity if extravasated

A

Vinca alkaloids

Anthracyclines

42
Q

Cisplatin toxicity

A

nephrotoxicity

43
Q

carboplatin toxicity

A

myelosuppression

44
Q

bleomycin toxicity

A

pulmonary toxicity

45
Q

doxorubicin toxicity

A

cardiotoxicity

46
Q

vincristine toxicity

A

neurotoxicity

47
Q

thalidomide toxicity

A

thromboembolism

48
Q

asparaginase toxicity

A

hypersensitivity

49
Q

bevacizumab toxicity

A

delayed wound healing

50
Q

cytarabine toxicity

A

cerebellar toxicity

51
Q

Describe the two forms of cardiotoxicity that can result from use of anthracyclines.

A
  • Acute: 24-72 hrs after administration, arrhythmias, pericarditis, myocarditis, subclinal
  • chronic: DOSE DEPENDENT, delayed by years, results in cardiomyopathy & associated heart failure
52
Q

What are two methods to reduce the risk of cardiotoxicity associated with doxorubicin use?

A
  • Risk can be mitigated by limiting lifetime doses

- Use of dexrazoxane: Reduces free radical formation in cardiac tissue, May reduce therapeutic effect of doxorubicin

53
Q

Explain the term secondary malignancy

A

Occur due to previous exposure to treatment (XRT or chemotherapy) for other cancers

54
Q

Are secondary malignancies harder or easier to tx compared to de novo malignancies?

A

harder

55
Q

MC secondary malignancies

A

acute leukemia

lymphoma

56
Q

What meds/agents are secondary malignancies mc associated with?

A

alkylating agents

etoposide

57
Q

Phase I goal of clinical trials

A

-assess safety
-assess dose ranges, schedule & efficacy
~10-20 pts who have NOT responded to other tx
-usually test agent in multiple types of CA

58
Q

Phase II goal of clinical trials

A
  • assess efficacy
  • assess safety & dosing
  • larger trial w/ more pts (20-40 more)
  • Focus on effect in patients with specific cancers who have not responded to other therapy
59
Q

Phase II goal of clinical trials

A
  • assess efficacy compared to standard treatment (RCT)
  • also assess safety
  • Larger than phase II trials
  • Enroll patients who are at the stage of a specific disease for which approval will be sought
60
Q

What is the name of the chromosomal mutation commonly seen in patients with CML? What does this mutation create?

A

-due to chromosomal translocation t(9:22) that forms the Philadelphia Chromosome -Gives rise to leukemia

61
Q

List 2 hormone sensitive cancers. How does this affect choice of therapy?

A
  • Breast Cancer
  • Prostate Cancer
  • Can use hormonal instead of chemotherapy (more specific therapy)
62
Q

Imatinib Indication

A

CML

63
Q

Thalidomide Indication

A

multiple myeloma

64
Q

Asparaginase Indication

A

ALL

65
Q

Fluorouracil/leucovorin Indication

A

colon cancer

66
Q

Trastuzumab Indication

A

Breast cancer

67
Q

Goserelin Indication

A

prostate cancer

68
Q

Paclitaxel Indication

A

lung cancer

Pharm III, Exam 3 Need to Knows (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions