Antineoplastic Pharmacology Flashcards
Prednisone, Desamethasone (Glucocorticoid)
CCS - G1
Mechanism: Induce apoptosis
Adverse effects: body fluid retention, hyperglycemia, weight gain, euphoria
Diethylsilbestrol, Testosterone (Gonadal hormones)
CCS - G1
Mechanism: Cytostatic
Adverse effects: Androgen - cholestatic jaundice
Estrogen - N/V, hypercalcemia
Tamoxifen (Gonadal Hormone Antagonist)
CCS - G1
Mechanism: Estrogen receptor blocker
Adverse effects: hot flashes, fluid retention
Flutamide (Gonadal Hormone Antagonist)
CCS - G1
Mechanism: androgen receptor blocker
Adverse effects: gynecomastia
Leuprolide/Goserelin (Gonadotropin-releasing Analog)
CCS - G1
Mechanism: decrease FSH/LH
Adverse effects: transient flare of symptoms in patients with bone metastasis
Anastrozole (Aromatase inhibitors)
CCS - G1
Mechanism: Inhibits formation of estrogen
Adverse effects: Nausea, asthenia, headache, hot flashes
L-Asparaginase
CCS - G1
Mechanism: deplete serum asparagine needed for growth
Adverse effects: Hypersensitivity, inhibit protein synthesis leads to decrease clotting factors, hypoalbuminemia
Methotrexate (antimetabolite)
CCS - S
Mechanism: analog of folic acid; inhibits DHFR –> depletes bases needed for DNA synthesis
Adverse effects: Myelosuppression, GI toxicity
Methotrexate Co-perscription
Folinic Acid help with toxicity
Methotrexate Overdose
Glucarpidase
6-Mercaptopurine (antimetabolite)
CCS - S
Mechanism: inhibit puren metabolism after activation by HGPRT; incorporated into DNA/RNA
Adverse effects: Bone marrow suppression
Cytarabine (antimetabolite)
CCS - S
Mechanism: activated by tumor cell kinases to inhibit pyrimidine metabolism
Adverse: bone marrow suppression, N/V
5-Fluorouracil (antimetabolite)
CCS - S
Mechanism: Inhibits thymidylate synthase –> thymine-less death
Adverse: diarrhea, bone marrow suppression
Bleomycin (antibiotics)
CCS - G2
Mechanism: Alters nucleis acid fxn via free radicals
Adverse: Pulmonary fibrosis, skin thickening
BONE MARROW SPARING
Etoposide
CCS - late S/early G2
Mechanism: Toposiomerase II inhibitor
Adverse: Neutropenia, N/V, diarrhea, hepatic dysfxn (high levels)
Vincristine, Vinblastine
CCS - M phase
Mechanism: Binds tubulin & blocks mitotic spindle assembly
Adverse: VC - neurotoxic; VB - bone marrow suppression
Paclitaxel
CCS - M phase
Mechanism: Block mitotic spindle disassembly (opposite of VC/VB)
Adverse: peripheral neuropathy, myelosuppression
Cisplatin
CCNS
Mechanism: Covalently bind DNA –> abnormal base pairing/strand breakage
Adverse: Peripheral neuropathy, renal insufficiency
BONE MARROW SPARING
Cyclophosphamide
CCNS
Mechanism: covalently bind DNA
**Activated by CytP450
Adverse: forms acrolein, causing bladder toxicity
Carmustine
CCNS
Mechanism: highly lipid soluble –> alkylating
Adverse:leukopenia, pulmonary fibrosis, N/V
Procarbazine
CCNS
Mechanism: Effects on DNA
**NEEDS activated by CytP450
Adverse: leukemia, bone marrow suppression, N/V
Doxorubicin
CCNS
Mechanism: Inhibit topoisomerase II + free radicals
Adverse: Myelosuppression, cardiotoxicity is dose-limiting
Dactinomycin
CCNS
Mechanism: inhibits DNA-dep RNA synthesis
Adverse: Bone marrow suppression
Daunorubicin
CCNS
Mechanism: Inhibit topoisomerase II + free radicals
Adverse: Myelosuppression, cardiotoxicity is dose-limiting
Mitomycin
CCNS
Mechanism: biotransform to alkylating agent
Adverse: Bone marrow suppression
Interferon-alpha
Mechanism: Inhibition of viral replication, suppress cell proliferation, augment lymphocyte cytotoxicity
Adverse: Myelosuppression, neurotoxicity
**Not commonly used unless maybe T cell lymphoma
Rituximab (monoclonal antibodies)
CCNS
Mechanism: Interacts with surface protein (CD20) on normal/malignant B lympocytes
Adverse: myelosuppression, hypersensitivity
Imatinib
CCNS
Mechanism: Inhibits abnormal tyrosine kinase made by Philadelphia chromosome
Adverse: diarrhea, nausea, cramps, fatigue
