cytotoxic Flashcards
Cyclophosphamide
Chlorambucil
•alkylating Nitrogen mustard derivative and is cell-cycle
nonspecific, producing DNA cross-linkages at any point in the cell cycle
Cyclophosphamide ADR
lymphoma, leukemia, bladder carcinoma, and squamous cell
carcinoma, and leukopenia from bone marrow suppression
Cyclophosphamide Hemorrhagic cystitis is associated with the increased risk of transitional cell carcinoma of the bladder and can occur in up to
40% of treated patients
if red blood cells are detected in the urine
cyclophosphamide must be discontinued
Cyclophosphamide Bladder toxicity
used to reduce this toxic effect
acrolein metabolite
mesna (sodium 2 mercaptoethanesulfonate)
Chlorambucil notable adverse effects
• Steroid-sparing agent in the treatment of vasculitis, Behcet’s disease, dermatomyositis,
histiocytosis X, and sarcoidosis
• Bone marrow suppression with leukopenia, oral ulcers, amenorrhea and azoospermia
Chlorambucil
In children with nephritic syndrome or adults with a seizure history, can cause
generalized
tonic-clonic seizures
S-phase specific antimetabolite
Methotrexate, hydroxyurea
Methotrexate competitively and irreversibly blocks dihydrofolate reductase from catalyzing the formation of
tetrahydrofolate, an important cofactor in
thymidylate and purine synthesis
Cumulative doses at or above?
can risk inducing liver fibrosis and cirrhosis;
4.0 grams
methotrexate use Uncommonly causes
acute pneumonitis and pulmonary fibrosis
Trimethoprim, the sulfonamides, and dapsone, which inhibit the folic acid metabolic pathway, when combined with methotrexate
can lead to hematologic toxicity
which drugs increase methotrexate levels by displacement of plasma proteins
Tetracyclines, phenytoin, phenothiazines,
chloramphenicol, NSAIDS, salicylates, and sulfonamides can all
greater risk of pancytopenia on MTXX
Patients with renal disease, those using
NSAIDS or TMP/SMX, and those with no
folate supplementation are a
Leukovorin (folinic acid) given under conditions of methotrexateinduced
myelosuppression with its ability
bypass dihydrofolate
reductase in the cell division pathway,