Extrapulmonary Small Cell Carcinoma Medication
- Author: Irfan Maghfoor, MD; Chief Editor: Jules E Harris, MD more...
Medication Summary
Medication used in the management of extrapulmonary small cell carcinoma includes chemotherapeutic agents to effect tumor shrinkage and induce remission as well as medication to reduce morbidity from treatment, malignancy, or both.
Antiemetic agents
Class Summary
Nausea and vomiting caused by antineoplastic agents is induced by stimulation of chemoreceptor trigger zone. This effect is mediated by central neurotransmitters (ie, dopamine and acetylcholine).
The severity of nausea and vomiting caused by antineoplastic agents varies with the agent or combination used, but it may be so disabling that patients occasionally decline continuation of chemotherapy. Appropriate prophylaxis and treatment of nausea and vomiting are therefore critical for administration of chemotherapy.
Metoclopramide (Clopra, Reglan, Maxolon, Octamide PFS)
Metoclopramide has central and peripheral antiemetic activity. In the CNS it acts on the chemoreceptor trigger zone while in the GI tract it stimulates acetylcholine release in the myenteric plexus.
Dexamethasone (Decadron)
Dexamethasone is a synthetic corticosteroid commonly used in combination with serotonin receptor antagonists or metoclopramide in prevention and treatment of chemotherapy-induced nausea and vomiting.
Ondansetron (Zofran)
Selective 5-HT3-receptor antagonist. Unclear whether effect is centrally and/or peripherally mediated. Used to prevent chemotherapy-induced nausea and vomiting.
Granisetron (Kytril)
Selective 5-HT3-receptor antagonist. Unclear whether effect is centrally and/or peripherally mediated. Used to prevent chemotherapy-induced nausea and vomiting.
Dolasetron (Anzemet)
Binds to 5-HT3 receptors located on vagal neurons in GI tract, blocking signal to VC, thus preventing nausea and vomiting.
Palonosetron (Aloxi)
Selective 5-HT3 receptor antagonist with long half-life (40 h). Indicated for prevention and treatment of chemotherapy-induced nausea and vomiting. Blocks 5-HT3 receptors peripherally and centrally in chemoreceptor trigger zone.
Antineoplastic agents
Class Summary
Chemotherapy forms the mainstay of management of extrapulmonary small cell carcinoma. Antineoplastic agents are used in potentially curative therapy in limited extrapulmonary small cell carcinoma in combination with radiation therapy, surgery, or both. In extensive extrapulmonary small cell carcinoma, chemotherapy is used for prolongation of survival or palliation of symptoms.
Antineoplastic agents interfere with cell division and growth. Some antineoplastic agents are cell-cycle dependent and phase specific, like antimetabolites (cytosine arabinoside, methotrexate), while others, like alkylating agents (cyclophosphamide), are not.
Etoposide (Toposar, VePesid)
Inhibits topoisomerase II enzyme leading to breakage of DNA strands. Etoposide is cell cycle specific and causes cell cycle arrest in late S and early G2 phase of cell cycle.
Cisplatin (Platinol)
Alkylating agent causing intrastrand and interstrand cross-linking of DNA, leading to strand breakage. Has broad range of antitumor activity. Use in testicular, ovarian, and transitional cell carcinomas.
Carboplatin (Paraplatin)
Analog of cisplatin (ie, platinum-salt alkylating agent). Has similar efficacy as cisplatin but with lower toxicity profile. Carboplatin is associated with less renal toxicity but enhanced myelosuppression compared to cisplatin. Mechanism of action for carboplatin is production of cross-links within and between strands of DNA.
Cyclophosphamide (Cytoxan, Neosar)
Chemically related to nitrogen mustards. As alkylating agent, mechanism of action of active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells.
Doxorubicin (Adriamycin, Rubex)
Inhibits topoisomerase II and produces free radicals, which may cause destruction of DNA. The combination of these 2 events can in turn inhibit growth of neoplastic cells.
Vincristine (Oncovin)
Inhibits tubulin polymerization during mitosis. G2 phase specific.
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