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Lecture Details[]

Shane Bullock; Week 10 MED1011; Pharmacology

Lecture Content[]

Alkylating agents (cyclophosphamide, cisplatin, ifosfamide) insert an alkyl group into DNA structure, cross links between adjacent bases (particularly guanine bases) as well as proteins. Causes stresses leading to strand breaks and apoptosis. Are generally cycle non-specific.

Cytotoxic antibodies (doxirubicin, mitomycin, daunorubicin) are too toxic to use in infectious disease therapy, cost vs benefit ratio is different in cancer. Inhibits transcription and translation processes.

Antimetabolites (methotrexate, 5-FU) substitute themselves in the DNA synthesis pathway. Block DNA synthesis and make molecule non-functional. Multiple pathways can be affected. They are cycle specific- S phase inhibitors. They affect the folate pathway and purine + pyramidine synthesis.

Mitotic poisons (vinca alkaloids, taxanes, etiposide) inhibit microtubule function, are necessary for formation of mitotic spindles or inhibit topsoisomerase. They are cycle specific.

Hormone antagonists such as SERMs (tamoxifen) are used when tumours require hormones for growth. Hormone antagonists can be glucocorticoids (cortisol, prednisolone), high doses leads to lysis of affected cells. Aromatase inhibitoris are anastrosole, androgen antagonists are cyproterone. GnRH analogue is goserelin.

Common adverse effects are organ toxicity (heart, nervous system, kidneys, urinary bladder).


Rang Ch 50[]