Nursing Pharmacology Chapter 33-34: Cancer Chemotherapy
Anti-Metabolite Practice Questions
Click on the correct answer.
Fludarabine (Fludara):Fludarabine is phosphorylated inside the cell by deoxycytidine kinase to monophosphate form with ultimate conversion to the triphosphate.
True
False
Fludarabine: mechanism(s) of anticancer action-
Fludarabine diphosphate (a metabolite) is an inhibitor of ribonucleotide reductase resulting in inhibition of deoxyribonucleotide triphosphates.
Fludarabine triphosphate is likely the main cytotoxic metabolite of fludarabine.
Both
Neither
Fludarabine triphosphate:
Competitor with deoxyadenosine triphosphate for DNA incorporation, serving thus as a highly effective chain Terminator.
Fludarabine triphosphate inhibits enzymes associated with DNA replication such as DNA polymerases, DNA ligase I, DNA primase and ribonucleotide reductase.
Both
Neither
Fludarabine exhibits anticancer activity against nondividing cells.
True
False
The principal anticancer effect of fludarabine may be related to its activation of an apototic mechanism.
True
False
Fludarabine incorporation into RNA:
Inhibits RNA function
Inhibits mRNA translation
Both
Neither
Fludarabine is considered highly active in treating patients with chronic lymphocytic leukemia.
True
False
Fludarabine:
Fludarabine is noted as active in follicular B-cell lymphoma which is resistant to standard treatment.
Fludarabine may be used for immunosuppression in nonmyeloablative allogenic bone marrow transplantation.
Both
Neither
Concerning fludarabine resistance:
Reduced intracellular formation of fludarabine triphosphate may occur as a result of reduced expression of deoxycytidine kinase.
Cross-resistance to other nucleoside analogues that depend on deoxycytidine kinase for activation is noted.
Agents exhibiting cross-resistance (deoxycytidine kinase activation dependency) include gemcitabine, cladribine, cytarabine and clofarabine.
A & B
B & C
A & C
A, B & C
Major side effect(s) due to fludarabine administration:
