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Pharm exam 3 > Cancer > Flashcards

Cancer Flashcards

1
Q

Cancer cell characteristics

A
  • uncontrolled cellular growth
  • ability to invade adjacent structures and/or travel to distant areas (metastases)
  • incapable of physiologic functions of the mature tissue of origin
  • altered proteins, enzyme systems, membrane characteristics, and cytogenetics
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2
Q

What is TNM?

A

Tumor-size
Nodal-spread –> local/systemic
Metastasis –> M0-no and M1-yes

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3
Q

What is adjuvant chemotherapy?

A

given after surgery to reduce risk of local and systemic recurrence

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4
Q

What is neoadjuvant chemotherapy?

A

given prior to surgical intervention to reduce tumor size or to remove micrometastases

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5
Q

What is cytotoxic chemotherapy?

A
  • 1st chemo
  • traditional
  • toxic to all cells but more specific for rapidly dividing cells like the GI tract, hair follicles, bone marrow
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6
Q

What is double time?

A

time needed for a tumor cell production to double in size

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7
Q

What gompertzian growth?

A

early growth is exponential but as tumor gets bigger, growth slows due to decreased nutrients/blood supply

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8
Q

what is log-kill hypothesis?

A

a given dose of chemotherapy kills the same fraction of tumor cells regardless of the size of the tumor at the time of treatment
-better efficacy in smaller tumors

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9
Q

What are the principles of cytotoxic chemotherapy?

A

combo chemo/regimen

  • good single-agent activity against tumor
  • different moa
  • different onsets of toxicities
  • max cell kill within toxicity limits
  • different moa to target a cancer cell in a diff way
  • decrease drug resistance
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10
Q

how are cytotoxic chemotherapy dosed?

A

dosed usually based on body surface area (BSA) and administered in cycles of 14, 21, or 28 days

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11
Q

What is dose density?

A

want to give the same amount of chemo at schedule time (same dose every 1 weeks)

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12
Q

what is dose intensity?

A

compressed dosing time to as short as possible

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13
Q

what are alkylating agents?

A
  • prevents cell division by cross-linking DNA strands and decreasing DNA synthesis
  • cell cycle non-specifc
  • myelosuppression is generally the dose-limiting toxicity
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14
Q

what are the types of cross-linking prevention?

A
  • monoalkylation
  • intercalation
  • crosslinked interstrand
  • crosslinked intrastrand
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15
Q

What are some alkylating agents?

A

cyclophosphamide, ifosfamide, cisplatin, carboplatin, oxaplatin

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16
Q

What common toxicities in alkylating agents?

A
  • n/v (acute/delayed)
  • myelosuppresion
  • alopecia
  • sterility/infertility
  • secondary malignancies
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17
Q

Cyclophosphamide/ifosfamide toxicities

A

need to be given together to prevent-
hemorrhagic cystitis (primarily ifosfamide) due to acrolein metabolite
-give mesna

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18
Q

Cisplatin toxicities

A

causes the most toxicities

  • nephrotoxicity
  • severe n/v (acute within 24 hrs and delayed up to 7 days later)
  • ototoxicity (mostly children)
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19
Q

Oxaliplatin toxicity

A

neuropathies (exacerbated by cold temperatures)

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20
Q

Antimetabolites

A
  • analogs of purines and pyrimidine compete with normal metabolites or falsely insert themselves for a metabolite normally incorporated into DNA or RNA
  • most commonly active in Sphase
21
Q

Antimetaboltes drugs

A

methotrexate, capecitabine, fluorouracil, cytarabine

*anti-folate

22
Q

Antimetabolites toxicities

A

common: myelosuppression, mucositis, mild n/v, diarrhea

23
Q

Methotrexate (MTX) toxicities

A
  • renal toxicities
  • Leucovorin rescue for high doses after 24 hrs to restart folic acid cycle
  • Cisplatin and MTX = never because of synergy effect and kill kidneys
24
Q

Cytarabine toxicities

A

high dose therapy: nervous system (cerebellar) toxicities of fine motor skills
-ocular irritation: steroid eye drops

25
Q

Fluorouracil toxicities

A

leucovorin- rescue dose only for MTX

26
Q

Capecitabine toxicity

A

hand-foot syndrome

27
Q

What are natural products of anti-neoplastic therapy?

A
  • antitumor antibiotics
  • plant alkaloids (vinca alkaloids, taxanes, topoisomerase 1 and 2)
  • marine-based products
  • enzymes
28
Q

Antitumor antibiotics drugs

A

anthracyclines- block DNA and RNA transcription
-Doxorubicin
mitomycin-crosslinks DNA (not used anymore)
dactinomycin-blocks RNA synthesis (kids only)
bleomycin-inhibits DNA synthesis (one cell-cycle specific agent)

29
Q

Antitumor antibiotics toxicities

A

n/v, alopecia, stomatitis, myelosuppression

30
Q

Bleomycin toxicities

A

antitumor antibiotics

-lung toxicity–> pulmonary fibrosis, interstitial pneumonitis

31
Q

Anthracyclines toxicities

A

antitumor antibiotics - Doxorubicin

-cardiotoxicity - specifically for CHF

32
Q

Antitumor antibiotics- myocardiotoxicity

A

dose-dependent

  • production of toxic free radicals, membrane lipid peroxidation leading to irreversible damage and replacement by fibrous tissue
  • risk factor: cumulative dose, patient age, concomitant chemo with known cardiotoxicity, rad therapy
  • early tox: HF can develop within 3 months following completion
  • late tox: sx may appear one decade later
  • give dexrazoxane–> edta like chelating agent, binds intracellular iron released following lipid peroxidation
33
Q

Natural product - microtubules agents

A
  • works at m phase
  • synthetic and semi-synthetic
  • different mechanism of actions–> prevent microtubule assembly(vinca alkaloids) or prevent microtubule disassembly (taxanes)
34
Q

Taxanes toxicities

A

plant alkaloids-microtubule toxicities

  • Docetaxel -neuropathies, peripheral edema, hypersensitivity reaction (to solvent for drug, not actual drug)
  • Paclitaxel- neuropathies, hypersensitivity rxn -premedicate with H1 and H2 blockers and steroid 30 mins prior
35
Q

Vinca Alkaloids toxicities

A

-all start with Vin
-Vincristine- neuropathies, severe constipation(anal tears)
Do not five intrathecal–>death
-Vinblastine
-Vinorelbine-myelosuppression

36
Q

Natural Products and Toxicities

A

Topoisomerase inhibitor 1+2- inhibit DNA repair mechanism

Irinotecan-diarrhea (I ran to the can)

  • due to cholinergic rxn
  • delayed-loperamide (16dosemax/day) and atropine

Etoposide-2nd cancers

Asparaginase- specifically for leukemias, hypersensitivity rxn, hyperglycemia, pancreatitis, coagulopathies
(ecoli derived)

37
Q

Natural products

Marine-based products

A

Eribulin- sea sponge
-microtubule-like agents
toxicities- fatigue, peripheral neuropathym, CINV-chemo induced n/v

Trabectedin-sea squirt

  • mechanism-somwhat like alkylating agent
  • toxicities- fatigue, hand-foot syndrome, CINV, hepatic damage
38
Q

Hormonal Tx

A
  • blocks production of hormones or hormone receptors in the body (breast and prostate
  • anti-estrogens
  • anti-androgens
  • luteinizing hormones-releasing hormones (LHRH) analogs
39
Q

SERM

A

Hormonal therapy
Tamaoxifen (antagonist)
-used in pre and postmenopausal women
-benefits:↓ odd of recurrence 37% and ↓15 yrs survival by 31%
-ADR: ↑ cataracts, endomentrial cancer, VTE, *CYP2D6 active metabolite, DDI with SSRI

40
Q

Aromatase Inhibitor

A

Hormonal therapy
Letrozolem anastrozole, exemestane
-postmeno preferred, premeno when combo with ovarian suppression
-benefits: post-aromatase inhibitor for 5 yrs ↓ recurrence
pre-varies add with OS
-ADR: osteoporosis, fractures, arthralgias

41
Q

Hormonal Therapy for Prostate Cancer

A

LHRH agonist: Leuprolide, goserelin, triptorelin
1st line therapy, inhibits negative feedback from releasing LH and FSH to stop stimulation of testes to produce testosterone
-tumor flare

LHRH antagonist
Degarelix
-directly inhibits pituitary from releasing LH and FSK
-2nd line therapy

Antiandrogens
Abiraterone, Bicalutamide, flutamide, nilutamide, enzalutamide, apalutamide

42
Q

ADR for hormonal therapy

A
  • decrease hormone production –> hot flashes for men and women
  • little protective effect on heart –> lipids will increase and increase risk of cardiac events when they’ll older
  • develop DB?
43
Q

Targeted Agents

A

identifies certain features of a cancer cell that makes it different from the normal cell

  • prevent tumor cells from entering cell cycle or target signals that trigger cancer growth, mets, and immorality
  • monoclonal antibodies-antibodies that match an antigen on the cancer cell surface
  • molecularly targeted therapies-blocks signaling inside the cell
44
Q

ADR Targeted Agents

A
  • hair depigmentation (stripes)
  • dysphonia
  • hypothyroidism
  • hypersenstivity rxn with all monoclonal antibodies
  • QTc prolongation
  • neuropathy
  • fatigue
45
Q

Targeted Agent Drugs

A

monoclonal antibodies- end in umab

small molecule targeted therapies - end in -nib

46
Q

What are target types?

A

VEGF(R) inhibitor- vascular endothelial growth factor
stops cancer angiogenesis
-causes hypertension (caution in DB), proteinuria, bleeding and impaired wound healing (stop pre/post surgery)
-HTN is a sign of efficacy
-ben, sun, pazo, regor

EGFR inhibitors- epidermal growth factor receptor

  • erlo, gef, alec, cet, panitu
  • acneiform rash - looks like acne.dry rash
  • treat with tetracycline, topical abx, and moisturizer
  • rash sign of efficacy

mTOR inhibitors0 mammalian target of rapamycin

  • ever, siro, tem
  • hyperglycemia, dyslipidemia, muscosal senstitivty, mouth ulcers
  • DDI with 3A4

BCR-ABL mutation inhibition- translocation of chromosome (give in small doses)

  • CYP 3A4 substrate except pona
  • ima 3A4 inhibitor and peripheral edema
  • ima, das, nilo, pona, bosu
  • low levels of constant nausea
47
Q

Specific Targets

A

CD20- ritx, ofatu, obin (DLBCL targets b cells)
-infusion rxn, myelosuppression

HER2 inhibition

  • traz. pert– cardiotoxicity
  • lapa= hand-foot syndrome, ddi with strong 3A4 inducer/inhibitor
48
Q

Target agent toxicities

A

monoclonal antibodies
-potential hypersensitivity rxn based on mAb origin

QT prolongation
-nilo, pazo, pona

Brentuximab
-neuropathy

Vemurafenib
-colitis

Bortezomib
-neuropathies

fatigue everyday!, hair thinning, low grade n/v/myelosuppression
-hypothyroidism (sun, pazo, rego)

Pharm exam 3 (1 decks)

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