Oncology II: Common Cancer Types and Treatment Flashcards by Jessica Weaver

skin cancer warning signs

ABCDE
Asymmetry
Border irregularities
Color inconsistent
Diameter >6mm
Evolving size, color, shape

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breast cancer risk factors

female
alcohol use
smoking
inc BMI
no exercise
poor nutrition

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why does an increased BMI present a risk factor for breast cancer development

as BMI increases, androgens stored in adipose are converted to estrogen via aromatase

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what syndrome places males at a risk for breast cancer

Klinefelter Syndrome where patients have XXY chromosome

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Patient is a pre-menopausal female with ER/PR + breast cancer. What is first line? Why?

SERM!
tamoxifen, bc it covers estrogen released from the ovaries which is the case in premenopausal
PLUS adjuvant for 5-10 years

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Patient is post-menopausal female with ER/PR+ breast cancer. What is first line?

Aromatase inhibitor
anastrozole
letrozole
exemestane
PLUS adjuvant for 5-10 years

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what medication is used as breast cancer prophylaxis in post-menopausal females who are ER/PR+

raloxifene

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tamoxifen BBW

endometrial cancer
uterine cancer

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tamoxifen
CI
ADE

CI in QT prolongation, warfarin use, DVT/PE hx, pregnancy
ADE: dec MBD –> + Ca and Vitamin D
hot flashes/night sweats

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treatment of choice for tamoxifen-induced hot flashes/night sweats

venlafaxine

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raloxifene BBW

increased risk of thromboembolism

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anastrazole ADE

inc risk of OP –> + Ca and Vit D
inc risk CVD

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which has a higher risk of CVD
SERM or aromatase inhibitors

aromatase inhibitor

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treatment of choice for HER2+ breast cancer

trastuzumab
pertuzumab

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what is the common toxicity with trastuzumab and pertuzumab for HER2+ breast cancer

cardiotoxicity

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tamoxifen counseling points

take Ca and Vitamin D to promote bone health
endometrial cancer risk
hot flashes/night sweats - venlafaxine an option
vaginal bleeding possible
decreased libido

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raloxifene counseling points

blood clot risk

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aromatase inhibitor counseling points

(anastrazole, letrozole, exemestane)
hot flashes/night sweats
inc risk CVD
muscle damage/pain

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prostate cancer treatment options

GnRH agonist PLUS antiandrogen
or
GnRH antagonist

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GnRH agonists
medications
use
ADE

leuprolide (Lupron depot)
Goserelin (Zoladex)
for prostate cancer with an antiandrogen
ADE: dec MBD (Ca, Vit D, DEXA scans), hot flashes/night sweats, weakness, impotence, bone pain, difficulty urinating

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antiandrogens
medications

first gen: bicalutamide
second gen: apalutamide
doralutamide
enzalutamide

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GnRH antagonists
medications
ADE

Degarelix (Firmagen SQ)
Relugolix (Orgovyx)
ADE: OP risk (Ca, Vit D, DEXA scans!)

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Which medications work in the M phase of the cell cycle

VT
Vinka alkaloids
- vincristine
- vinblastine

Taxanes
- paclitaxel
- docetaxel

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Which medications work on the G1 phase of the cell cycle?

asparginase
interferons
steroids

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Which medications work on the S phase of the cell cycle (DNA replication)?

antimetabolites - MTX - 5-FU - capecitabine Topo I inhibitors - irinotecan - topotecan

Medications that work on G2 phase of cell cycle?

Topo II inhibitors - etoposide - bleomycin

max life dose of bleomycin

400 units per life

max dose of vincristine

2mg/dose

cell cycle independent agenst

alkylating agents - carmustine - cyclophosphamide - ifosfamide anthracyclines - doxorubicin - mitoxantrone platinum compounds - cisplatin - carboplatin

cyclophosphamide and ifosfamide toxicity concern and prophylaxis?

hemorrhagic cystitis mesna!

BSA equation

square root of (cm x kg) / 3600

alkylating agents CC dependent or independent meds BBW ADE

cc independent busulfan, cyclophosphamide, ifosfamide BBW: hemorrhagic cystitis (cyclo and ifos) myelosuppression ADE: SJS/TEN, infection reactivation (HBV, CML, TB, HCV), hepatotoxicity, emesis, mucositis, alopecia, neurotoxcity, secondary malignancy

mesna use MOA

cyclophosphamide and ifosfamide induced hemorrhagic cystitis cyclophsophamide is metabolized to acrolein which concentrates in bladder; mesna prevents concentration in bladder

platinum-based chemo agents cc dep or independent? medications ADE

cc independent cisplatin, carboplatin SE cisplatin: nephro and oto toxicity, highly emetogenic, max is 100mg/m2/cycle to protect kidneys

__________ is used for cisplatin-induced nephrotoxicity prophylaxis

amiphostine

anthracyclines cc dep or indep medications pearls BBW

cc independent doxorubicin: lifetime dose 450-550 mg/m2, consider dexrazoxazone at doses >300mg/m2, RED discoloration of bodily fluids BBW: cardiotoxicity, vesicant, myelosupp, secondary malignancy mitoxantrone: BLUE discoloration of bodily fluids BBW: cardiotoxicity, myelosupp, secondary malignancy

Irinotecan MOA SE BBW

Topo-I - inhibitor cell cycle S SE: N/V/D, alopecia, diarrhea, abd pain, acute cholinergic sx BBW: myelosupp, diarrhea (early and late)

Patient presents with irinotecan-induced delayed diarrhea. Treatment?

loperamide

Patient presents with irnotecan-induced cholinergic symptoms (flushing, sweating, diarrhea, cramps). Treatment?

atropine

Etoposide MOA administration BBW ADE

MOA: Topo II inhib in G2 phase of cell cycle admin: infuse over 30-60 min to prevent hypotension, IV prep must be

is bleomycin myelosuppressive

bleomycin MOA administration BBW ADE

Topo II inhibitor in G2 phase of cell cycle **NEED TEST DOSE**, max is 400 units/life BBW: pulmonary fibrosis, anaphylaxis ADE: HSRxn, pneumonitis, mucositis, hyperpigmentation, fever, chills, N/V (mild)

vincristine MOA administration ADE pearls

vinka alkaloid in M phase of cell cycle administered IV! Max is 2mg/dose ADE: vesicant, CNS toxicity, peripheral neuropathy C for CNS toxicity

vinblastine MOA administration ADE pearls

vinka alkaloid in M phase of cell cycle administered IV! ADE: B for bone marrow suppression

Which chemo agents are NOT myelosuppressive

bleomycin vincristine

vinka alkaloids BBW

IV administration only vesicants peripheral sensory neuropathies (parasthesias) autonomic neuropathy (gastroparesis, constop), SIADH

If a patient is receiving paclitaxel they should be pre-treated with _______________________

diphenhydramine, steroids and H2RA

If a patient is receiving docetaxel they should be pre-treated with _______________________

steroids x3 days starting one day before docetaxel

5-FU MOA given with __________ to inc efficacy antidote BBW SE

pyrimidine analog/antimetabolite in the S phase of cell cycle given with leucovirin to increase efficacy antidote = uridine triacetate BBW inc INR SE: hand-foot-mouth, mucositis, diarrhea

capecitabine MOA CI SE BBW antidote

pyrimidine analog/antimetabolite in the S phase of cell cycle po prodrug of 5-FU CI CrCl <30mL/min SE: hand-foot-mouth, mucositis, diarrhea BBW: inc INR antidote: uridine triacetate

paclitaxel and docetaxel MOA BBW SE DDI

taxanes in M phase of cell cycle BBW: severe HSRxn, myelosuppression, fluid retention (docetaxel) SE: peripheral sensory neuropathy, myalgias, arthralgias, alopecia, hepatotoxicity DDI: platinum-based (cisplatin and carboplatin) dec taxane eliminiation --> need to reduce taxane dose

what is an additional benefit of pretreating docetaxel with steroids other than to curb HSRxn

aids in reducing fluid retention ADE

Patient is on paclitaxel and provider wants to initiate cisplatin. How should dose be adjusted? A. discontinue taxane B. patient will require an increased cisplatin dose C. patient will require and increased paclitaxel dose D. patient will require a decreased paclitaxel dose

D. patient will require a decreased paclitaxel dose Paclitaxel elimination is inhibited by cisplatin and other platinum, requiring a decreased paclitaxel dose

Patient initiated on 5-FU and develops toxicity. What could be a possible explanation? A. G6PD deficiency B. HLA-B*5701 gene mutation C. DPD deficiency D. renal insufficiency

C. DPD deficiency

When do we need to dose adjust taxanes paclitaxel and docetaxel

hepatic impairment

methotrexate doses >/= ______________ require the addition of ___________

500mg/m2 leucovirin

Why is sodium bicarb added in methotrexate treatment

to alkalinize urine and decrease nephrotoxicity risk

Avoid MTX in patients with _________ due to ________

3rd spacing (edema, ascites, pleural effusions) decreased CL

Patient initiated on MTX develops AKI. What is the antidote? A. glucarpidase (Voraxane) B. leucovirin C. uridine triacetate D. NS E. lactated ringers

A. glucarpidase (Voraxane)

Doses of MTX are higher or lower in chemo than in RA?

higher

Match the McAb to the MOA Bevacizumab (Avastin) EGFR-i Trastuzumab (Herceptin) CD20-i Cetuximab (Erbitux) VEGF-i Rituximab (Rituxan) anti-HER2 Pembrolizumab (Keytruda) PD-L1 i Nivolumab (Opdivo)

Trastuzumab (Herceptin) anti-HER2 Bevacizumab (Avastin) VEGF-i Cetuximab (Erbitux) EGFR-i Rituximab (Rituxan) CD20-i Pembrolizumab (Keytruda) PD-L1 i Nivolumab (Opdivo) PD-L1 i

What drug am I? I need to be pre treated with benadryl Please test for EGFR gene expression first BBW severe/fatal infusion reaction, cardiac arrest Can cause an acneiform rash that, if occurs in first two weeks, is a sign treatment will be successful! Avoid sunlight

cetuximab

What drug am I? I need to be pre-treated with benadryl, steroids and APAP BBW: Hep B reactivation, PML, SJS/TEN, infusion reaction Check for Hep B before starting me!

Rituximab (Rituxan)

What drug am I? I cannot be given 28 days before or after a surgery because I will impair wound healing and have BBW for severe fatal bleeding, GI perforation and wound opening. Monitor for proteinuria, HTN, nephrotic syndrome, HF and thrombosis

Bevacizumab (Avastin)

What drug am I? You must use a 0.22 micron filter with me I have BBW for HF, embryo-fetal death, birth defects, infusion reactions, pulm toxicty, hepatotox, interstital lung disease and pneumonitis

Trastuzumab (Herceptin)

MTX BBW

myelosupp aplastic anemia renal damage hepatotoxicity interstitial pneumonitis SJS/TEN GI tox immunosuppression TLS teratogenicity/fetal death

MTX DDI A. NSAIDs, PPIs, cephalosporins, salicylates, probenacid B. NSAIDs, H2RA, beta lactams, salicylates, probenacid, sulfonamides C. NSAIDs, PPIs, beta lactams, salicylates, probenacid, sulfonamides D. NSAIDs, H2RA, cephalosporins, salicylates, probenacid, sulfonamides

C. NSAIDs, PPIs, beta lactams, salicylates, probenacid, sulfonamides

In order to use tyrosine kinase inhibitors, patients must be positive for ________________.

philadelphia chromosome (BCR-ABL)

Oral chemo agents imatinib (Gleevec) and Capecitabine (Xeloda) must be given with or without food?

with food

Common TK-inhibitor toxicities

heart - QTp skin - acneiform rash, SJS/TEN lg int - diarrhea hand-foot syndrome liver - 3A4 substrates (DDI and toxicities)

What cancer are TK-i s commonly used in

CML

Oncology II: Common Cancer Types and Treatment Flashcards

Lung Cancer Skin Cancer Breast Cancer Prostate Cancer Cell cycle treatments BSA calculations Other Medicatoins McAbs