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nurs 366: pathopharm ii > ONCOLOGY - cancer treatments > Flashcards

ONCOLOGY - cancer treatments Flashcards

EXAM 2 content (39 cards)

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1
Q

what factors indicate the prognosis?

A
  • response to treatment
  • health & age
  • type, location, stage & grade
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2
Q

what is the goal of treatment?

A

cure, remission, control, palliation
- control: cant eradicate BUT responds to anticancer treatments

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3
Q

what are the different types of treatments?

A

surgery, chemotherapy, radiation, immunotherapy, & hormonal therapy
- combination is used mostly

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4
Q

what is the purpose of surgery?

A
  • prevention
  • diagnosis –> biopsy & clinical staging
  • cure / control of cancer
  • palliation of symptoms
  • rehab
  • supportive care
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5
Q

how does radiation therapy work? what is the goal? what is the primary cause of side effects & toxicity?

A

HOW IT WORKS: uses high energy beams/waves –> absorbed in tissue –> produces ions in cells –> breaks chemical bones in DNA –> DNA damaged –> cell death

GOAL: remove cancer w/o toxicity or damage to norm structures – can define area
- sometimes have to do whole body, esp for leukemia

damage to normal cells = primary cause of side effects & toxicity

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6
Q

how does immunotherapy work? what is within immnotherapy

A

HOW IT WORKS:
- boosting / manipulating immune system + create environment not good for cancer cell growth
- attacking cell directly
- using: cytokines, vaccines & monoclonal antibodies

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7
Q

how do monoclonal antibodies work?

A

ALL END IN -MAB
- made in the lab –> binds to antigens on surface of cancer cells
- binds only to ONE antigen
- alone or carries drugs, toxins or radioactive substances directly to cancer cells

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8
Q

what cancers is hormonal therapy used for? why?

A

prostate & breast cancer
- prostate cancers develop in ANDROGEN DEPENDENT epithelium, androgen sensitive – produced by testes, adrenal glands & prostate cancer cells
- breast cancers depend on ESTROGEN

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9
Q

what is the goal of hormonal therapy when combating prostate cancer?

A

ANDROGEN DEPRIVATION
- castration = orchiectomy: surgical removal of testes w or w/o prostatectomy
- drugs to deprive prostate cancers – can produce chemical castration similar to orchiectomy

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10
Q

what are the 3 drug classes for hormonal (endocrine) therapy that combat prostate cancer?

A
  • Gonadotropin releasing hormone (GnRH) agonists
  • GnRH antagonists
  • Androgen receptor blockers
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11
Q

what is the examplar drug for GnHR agonist? administration?

A

LEUPROLIDE – SQ & IM

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12
Q

how does LEUPROLIDE work?

A

a synthetic analogy of GnRH = luteinizing hormone releasing hormone (LHRH)

acts on pituitary –> stimulated release of interstitial cell hormone (ISCH) –> initially testes increase production of testosterone –> might have transient flare of prostate cancer symptoms –> as time goes on GnRH receptors become desensitized & ICSH release –> testosterone production decreased

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13
Q

what is the exemplar drug of GnRH antagonist? administration?

A

DEGARELIX – SQ

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14
Q

how does DEGARELIX work?

A

blocks GnRH receptors in the anterior pituitary –> decrease release of luteinizing & follicle stimulating hormone –> decr stimulus for testosterone production –> decr production of androgens

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15
Q

what is the biggest difference between GnRH agonist & antagonist?

A

GnRH antagonist (DEGARELIX) does NOT cause initial surge in testosterone production & symptom flare

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16
Q

what is the exemplar drug for androgen receptor blockers? when should we use this medication? administration?

Study These Flashcards
A

FLUTAMIDE – oral
- only for advanced cancer WITH surgery or WITH GnRH medicine

17
Q

how does FLUTAMIDE work?

Study These Flashcards
A

blocks androgen receptors in tumor cells –> prevents binding of testosterone to prostate cancer cells + small decr in androgen production by adrenal gland

18
Q

what are the adverse effects of hormonal therapy for prostate cancer?

Study These Flashcards
A

systematic effects from decreased testosterone
- hot flashes
- reduced libido
- ED
- gynecomastia
- decr muscle mass
- decr bone mass w incr risk of fractures

19
Q

what hormonal therapy classes are used for breast cancer?

Study These Flashcards
A

antiestrongens & aromatase inhibitors

20
Q

what is the exemplar drug for antiestrogen’s? administration?

Study These Flashcards
A

TAMOXIFEN – oral

21
Q

how does TAMOXIFEN work?

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A

a prodrug undergoes active metabolites –> blocks receptors of estrogen receptor positive breast cancer cells –> prevents activation of ESTRADIOL (principle endogenous estrogen) –> decr tumor cell differentiation

22
Q

what are the adverse effects of TAMOXIFEN?

Study These Flashcards
A
  • hot flashes
  • fluid retention
  • vaginal discharge
  • n/v
  • menstrual irregularities
23
Q

what kind of cancer can TAMOXIFEN increase risk for? why? what do we to avoid when taking this drug?

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A

endometrial cancer
- drug acts a receptor AGONIST to uterus –> proliferation of endometrial tissue

AVOID GETTING PREGGY

24
Q

what is the exemplar drug for aromatase inhibitors? administration? who specifically are we giving it to? why?

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A

ANASTROZOLE – oral
- post menopausal women – they block estrogen made by ovaries, thats why we do not give to premenopausal

25
how does ANASTROZOLE work?
androgens = precursor of ALL estrogen - blocks production of estrogen from androgenic precursors --> depriving breast cancer cells of estrogen needed for growth
26
what are the adverse effects of ANASTROZOLE?
- muscle pain - asthenia = weakness - headache - menopausal symptoms (hot flash & vag dryness) - incr fract risk
27
what is chemotherapy? what does it do? what are the different types of chemotherapies?
chemotherapy = cytotoxic drugs = toxic to living cells --> kills norm & cancer cells - usually gives in combo to attack a cancer from different weaknesses at the same time - COMPLICATION: death of rapidly dividing cells that are NOT cancerous - induction chemotherapy = first cancer of treatment, shrinks or disappears tumor - adjuvant chemotherapy = in conjunction w primary cancer treatment -- radiation / surgery - neoadjuvant therapy = first step to shrink a tumor BEFORE main treatment
28
there are many precautions when giving chemotherapy, which drugs do we need to be careful the most, why?
- antineoplastic drugs: mutagenic, teratogenic, & carcinogenic -- local injury to skin, eyes & mucous membranes - IV vesicants: extravasation can cause severe local injury --> use central IVs
29
what are the safe handling procedures of chemotherapy?
- precautions to take during preparation, administration & handling bodily fluids for 48 hrs AFTER drug administration - double chemotherapy gloves - protective gowns - face shields
30
what are the two major groups of chemotherapy?
- cell cycle phase NONspecific - cell cycle phase SPECIFIC
31
what medication groups are under cell cycle phase non specific (chemotherapy)?
- alkylating agents - platinum compounds - antitumor antibiotics
32
what medication groups are under cell cycle phase SPECIFIC (chemotherapy)?
- antimetabolites - mitotic inhibitors - topoisomerase inhibitors
33
how does alkylating agents work? (cell cycle phase nonspecific) cytocidal? cytotastic?
breaks double stranded helix in DNA --> damage DNA - if does not repair = cytocidal - will die if they try to divide = cytostatic
34
how does platinum compounds work? (cell cycle phase nonspecific)
binds to DNA & RNA --> miscoding of information + inhibition of DNA replication --> cell death - similar to alkaline agents
35
how does antitumor antibiotics work? (cell cycle phase nonspecific)
ONLY used for cancer - binds directly to DNA --> inhibits DNA synthesis - interferes with RNA transcription (1st step in gene expression) --> no cell division --> cell death
36
when does DNA synthesis occur?
when chromosomes are duplicated by cell to prep for mitosis
37
how does antimetabolites work? (cell cycle phase SPECIFIC)
acts on S phase -- mimics natural substances & interferes with enzyme function or DNA synthesis - interferes with purine metabolism: building blocks of nucleic acids - interferes with pyrimidine metabolism: building blocks of nucleic acids - interferes with folic acid metabolism - interfere with DNA synthesis ALL LEADS TO: blocking DNA synthesis --> cell death
38
how does antimitotics aka mitotic inhibitors work? (cell cycle phase specific) what does the 2 drug classes do?
TAXANES -- inhibits mitosis by acting on microtubules - interferes w mitosis during late G2 phase --> inhibits cell division + microtubule stability --> altering cancer function VINCA ALKALOIDS -- inhibits mitosis by acting on microtubules - disrupts/blocks assembly of microtubules in M phase --> inhibits mitosis
39
how does topoisomerase inhibitors work? (cell cycle phase specific)
normally -- topoisomerases break & rejoin DNA strands that are needed for cell division & proliferation topoisomerase inhibitors STOPS that --> cell death

nurs 366: pathopharm ii (30 decks)

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