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

ONCOLOGY - cancer treatments Flashcards

EXAM 2 content

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?

A

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

17
Q

how does FLUTAMIDE work?

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?

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?

A

antiestrongens & aromatase inhibitors

20
Q

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

A

TAMOXIFEN – oral

21
Q

how does TAMOXIFEN work?

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?

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?

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?

A

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

25
Q

how does ANASTROZOLE work?

A

androgens = precursor of ALL estrogen
- blocks production of estrogen from androgenic precursors –> depriving breast cancer cells of estrogen needed for growth

26
Q

what are the adverse effects of ANASTROZOLE?

A
  • muscle pain
  • asthenia = weakness
  • headache
  • menopausal symptoms (hot flash & vag dryness)
  • incr fract risk
27
Q

what is chemotherapy? what does it do? what are the different types of chemotherapies?

A

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
Q

there are many precautions when giving chemotherapy, which drugs do we need to be careful the most, why?

A
  • antineoplastic drugs: mutagenic, teratogenic, & carcinogenic – local injury to skin, eyes & mucous membranes
  • IV vesicants: extravasation can cause severe local injury –> use central IVs
29
Q

what are the safe handling procedures of chemotherapy?

A
  • precautions to take during preparation, administration & handling bodily fluids for 48 hrs AFTER drug administration
  • double chemotherapy gloves
  • protective gowns
  • face shields
30
Q

what are the two major groups of chemotherapy?

A
  • cell cycle phase NONspecific
  • cell cycle phase SPECIFIC
31
Q

what medication groups are under cell cycle phase non specific (chemotherapy)?

A
  • alkylating agents
  • platinum compounds
  • antitumor antibiotics
32
Q

what medication groups are under cell cycle phase SPECIFIC (chemotherapy)?

A
  • antimetabolites
  • mitotic inhibitors
  • topoisomerase inhibitors
33
Q

how does alkylating agents work? (cell cycle phase nonspecific) cytocidal? cytotastic?

A

breaks double stranded helix in DNA –> damage DNA
- if does not repair = cytocidal
- will die if they try to divide = cytostatic

34
Q

how does platinum compounds work? (cell cycle phase nonspecific)

A

binds to DNA & RNA –> miscoding of information + inhibition of DNA replication –> cell death
- similar to alkaline agents

35
Q

how does antitumor antibiotics work? (cell cycle phase nonspecific)

A

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
Q

when does DNA synthesis occur?

A

when chromosomes are duplicated by cell to prep for mitosis

37
Q

how does antimetabolites work? (cell cycle phase SPECIFIC)

A

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
Q

how does antimitotics aka mitotic inhibitors work? (cell cycle phase specific) what does the 2 drug classes do?

A

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
Q

how does topoisomerase inhibitors work? (cell cycle phase specific)

A

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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