Drug MOA Flashcards
What is the mechanism of increased uric acid in cancer patients?
Tumor Lysis Syndrome.
- tumor intracellular components like Ca+, K+, Phos+, and nucleic acids spill out
- purines from the nucleic acids get converted into uric acid by xanthine oxidase
Neupogen
Filgrastim
Colony Stimulating Factor will stimulate production of WBC to treat neutropenia
Neulasta
Pegfilgrastim
Colony Stimulating Factor will stimulate production of WBC to treat neutropenia
Emend
Aprepitant (PO)
Fosaprepitant (IV)
Substance P / Neurokinin 1 receptor antagonist thid mechanism augments the antimetic activity of both 5-ht-3 RA and corticosteroids
Zuplenz film
Ondansetron
5-HT-3 RA that blocks serotonin both on peripheral vagal nerves and central chemoreceptor trigger zone
Sancuso
Granisetron
5-HT-3 RA that blocks serotonin both on peripheral vagal nerves and central chemoreceptor trigger zone
Aloxi
Palonosetron
5-HT-3 RA that blocks serotonin both on peripheral vagal nerves and central chemoreceptor trigger zone
Decadron
Dexamethasone
Corticosteroid for CINV
Compazine
Prochlorperazine
DA receptor antagonist that blocks DA in CNS that is a part of the chemo trigger zone
Phenergan
Promethazine
DA receptor antagonist that blocks DA in CNS that is a part of the chemo trigger zone
Reglan
Metoclopramide
DA receptor antagonist that blocks DA in CNS that is a part of the chemo trigger zone
Zyprexa
Olanzapine
DA receptor antagonist that blocks DA in CNS that is a part of the chemo trigger zone
Marinol
Dronabinol
activating cannabinoid receptors in the CNS and inhibiting the vomiting control in the medulla oblongata
Ativan
Lorazepam
enhances GABA (an inhibitor neurotransmitter) to decrease neuronal excitability that will suppress anticipatory N/V
Miacalcin
Calcitonin
inhibits bone resorption
(for moderate to severe Hypercalcemia)
Ca > 12 mg/dL
Zometa
Zoledronic acid IV 4 mg (may repeat dose in 7 days)
Bisphosphonate that blocks osteoclast mediated bone breakdown
Osteoporosis brand = Reclast dosed at 5 mg yearly
Xgeva
Denosumab 120 mg SC x3 for 1st month, then monthly
monoclonal antibody that blocks interaction between RANKL and RANK to prevent osteoclast formation
for moderate to severe hypercalcemia (Ca > 12 mg/dL)
Osteoporosis brand name is Prolia 60 mg SC every 6 months
Tamoxifen
Selective-Estrogen Receptor Modulator for ER+/PR+ breast cancers
binds to estrogen receptors on tumors to prevent growth from estrogen binding and feeding the tumor
Raloxifene
Selective Estrogen Receptor Modulator used for prophylaxis in select post-menopausal women
Fulvestrant
Selective Estrogen Receptor Degrader that causes the estrogen receptors to downregulate and degrade
Arimidex
Anastrozole
Aromatase inhibitor that treats postmenopausal breast cancer by blocking the peripheral conversion of of androgens to estrogens
***does not block ovarian estrogen production!
Letrozole
Aromatase inhibitor that treats postmenopausal breast cancer by blocking the peripheral conversion of of androgens to estrogens
***does not block ovarian estrogen production!
Trastuzumab
Herceptin
binds to HER2 (oncogene) to block the dimerization to block the amplified cell growth
Lupron Depot
Leuprolide
GnRH Agonist or LH agonist that initially increase LH to increase testosterone but eventually will create a negative feedback loop to decrese testosterone production
Zoladex
Gosrelin
GnRH Agonist or LH agonist that initially increase LH to increase testosterone but eventually will create a negative feedback loop to decrese testosterone production
Degarelix
GnRH Antagonist causing a rapid decrease in testosterone production
Relugolix
GnRH Antagonist causing a rapid decrease in testosterone production
Bicalutamide
Antiandrogens 1st gen
MUST be used with GnRH
competivitely blocks testosterone
Bi Ni Flu
Nilutamide
Antiandrogens 1st gen
MUST be used with GnRH
competivitely blocks testosterone
Bi Ni Flu
Flutamide
Antiandrogens 1st gen
MUST be used with GnRH
competivitely blocks testosterone
Bi Ni Flu
Apalutamide
Antiandrogen 2nd gen
do not cause upregulation of androgren receptors can be used as single treatment
2AED
Darolutamide
Antiandrogen 2nd gen
do not cause upregulation of androgren receptors can be used as single treatment
2AED
Enzalutamide
Antiandrogen 2nd gen
do not cause upregulation of androgren receptors can be used as single treatment
2AED
Taxanes (Paclitaxel, Docetaxel)
Block M-phase (mitosis) of cell cycle
Vinca Alkaloids (Vincristine, Vinblastine)
Block M-phase (mitosis) of cell cycle
Asparaginase
Block G1 (making of DNA/RNA/proteins) of cell cycle
Antimetabolites (Methotrexate, Fluoroucil, Capecitabine)
Block S phase (replication) of cell cycle
AT in replicATe
Topoisomerase 1 inhibitors (Irinotecan, Topotecan)
Block S phase (replication) of cell cycle
AT in replicATe
Topoisomerase 2 inhibitors (bleomycin, etopodise)
block DNA coiling and uncoiling causing the DNA to break in G2 phase (growth of DNA)
Alkylating Agents (cyclophosphamide, ifosfamide)
independent of cell cycle
Anthracyclines (Doxorubicin, Mitoxantrone)
independent of cell cycle
Platinium Compounds (Cisplatin, Carboplatin)
independing of cell cycle
Cyclophosphamide
Alkalyating agent that is independent of cell cycle that cross-link DNA strands to inhibit proteina and DNA synthesis
***hemorrhagic cystitis
Ifosamide
Alkalyating agent that is independent of the cell cycle that cross-links DNA strands to inhibit protein and DNA synthesis
***hemorrhagic cystitis = Mesna
Carmustine
Alkalyating agent that is independent of the cell cycle that cross links DNA
***pulmonary toxicity
Busulfan
Alkalyating agent that is independent of the cell cycle that cross links DNA
***pulmonary toxicity
Cisplatin
Platinum Compounds bind and cross link DNA strands in all cell cycle
Oxaliplatin
Platinum Compound bind and crosslink DNA strans in all cell cycle
Carboplatin
Platinum Compound bind and crosslink DNA strands in all cell cycle
Doxorubicin
Anthracycline that intercalates into DNA and inhibits Topo 2 and creates oxygen free radicals that damage cells
**administer with Dexrazoxane to diminish cardiotoxicity
Mitoxantrone
Anthracycline that intercalates into DNA and inhibits Topo 2 and creates oxygen free radicals that damage cells
**administer wiht Dexrazoxane to diminish cardiotoxicity
Irinotecan
Topo 1 inhibitor blocking phase S (replication) coiling and uncoiling of DS DNA. This prevents religation of the DS DNA
SE: DIARRHEA and myleosuppresion
Bleomycin
Topo 2 inhibitor blocking phase G2 coiling and uncoiling of DS DNA to prevent religation of the DS DNA
SE: Pulmonary fibrosis
Hypersensitivity rxn
Vincristine
Vinca Alkaloid that blocks the MICROTUBULES during M phase
SE: neuropathy
vesicant
constipation
Vinblastine
Vinca Alkaloid that blcks MICROTUBULES during M phase
SE: myleosuppression
neuropathy
vesicant
Paclitaxel
Taxane that inhibit microtubule function in M phase
SE: neuropathy
hypersensitivity rxn
myelosuppression
Docetaxil
Taxane that inhibit microtubule function in phase
SE: neuropathy
hypersensitivity rxn
myelosuppression
Fluorouracil
inhibit pyrimidine synthesis by acting as uracil incorporating itself into RNA to inhibit cell growth and replication in S phase
SE: myleosuppression, diarrhea, mucositis, hand foot syndrome
**look for DPD deficiency
Capecitabine
Prodrug of Fluorouracil
inhibit pyrimidine synthesis by acting as uracil incorporating itself into RNA to inhibit cell growth and replication in S phase
SE: hand-foot syndrome
diarrhea
mucosistis
myelosuppression
**look for DPD deficiency
Trexall
Methotrexate
Folate antimetabolite that blocks pyrine and pyrimidine biosynthesis during the S phase
SE: Myelosuppression, heptotoxocity, nephrotoxicity, GI toxicity (mucositis), Teratogenicity