Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

52 Cards in this Set

  • Front
  • Back
pt. w/chemo for Hodgkins develops symptoms of schizophrenia; which drug is causing?
-prednisone=CNS toxicity=psychosis
Cancer cells lacking hypoxanthine-guanine phosphoribosyl transferase (HGPRTase)are resistant to ?
-6-mercaptopurine and 6-thioguanine

-The enzyme HGPRTase converts 6-MP and 6-TG to a nucleotide form which inhibits purine synthesis and thus blocks
DNA/RNA synthesis
-medical use?
-Cyclophosphamide used to treat non-Hodgkins lymphoma, breast and ovarian carcinomas
-MOA = activated by CYP450 to a metabolite which covalently x-links
DNA strands at guanine N-7
-S/E = causes sterile hemorrhagic cystitis; alkylating agents like cyclophosphamide can cause myelogenous (granulocytic) leukemia
pt to be tx w/chem/cyclophosphamide. pt is also receiving tx for gout. which gout drug would inc the toxicity of cyclophosphamide?
-allopurinol prolongs the half-life of cyclophosphamide
Drug interactions with Allopurinol
a.alluopurinol inhibits xanthine oxidase to prevent the formation of uric acid)

b.allopurinol often used after tx of hematologic cancers to prevent hyperuricemia after tumor cell lysis

c.allopurinol inhibits the metabolism of 6-mercaptopurine (6-MP) by xanthine oxidase,so need to reduce dose of 6-MP to 25% of normal dose in patients on allopurinol
d.Need to dec dose of immunosuppressive drug azathioprine by 25% of normal when given to a patient taking allopurinol because azathioprine is metabolized to 6-MP
Drugs that interfere w/microtubule fxn?
-vincristine:Vinblastine binds to tubulin and blocks the ability of tubulin to polymerize intomicrotubule = mitotic arrest in metaphase

-placlitaxel (taxol)
Paclitaxel used to tx ovarian and breast cancer
-MOA = binds to microtubules of mitotic spindle to hyperstabilize them so that they cannot break down in anaphase, get mitotic arrest
dactinomycin (actinomycin D)
-MOA of dactinomycin (actinomycin D)=binds tightly to double-stranded DNA between G-C pairs to inhibit all forms of DNA-dependent RNA synthesis, esp. mRNA synthesis

-used for the tx of Wilm’s tumor
Doxorubicin and Danurubicin
= anthracycline antibiotics
-MOA = intercalation into DNA - inhibits synthesis of DNA/RNA
Doxorubicin and Danurubicin
= anthracycline antibiotics
-toxicity = forms free radicals and oxygen radicals causing cardiac toxicity via
membrane damage
-used to tx leukemias and sarcomas
-forms a polyglutamate adduct which is important for its duration of action
-MOA = a folic acid antagonist which binds to DHF reductase, interferes w/ synthesis of thymidylate, purine nucleotides and the AA’s serine and methionine

=inhibition of synthesis of DNA, RNA and proteins
-causes of resistance?
- decreased drug transport
- altered DHFR
- increased activity of DHFR
- decreased polyglutamate formation
-bone marrow depression
pt tx w/methotrexate develops bone marrow dep. hot to tx?
-“leucovorin rescue”
=tx w leucovorin (folinic acid) to reverse bone marrow

-Normal cells can take up leucovorin, but tumor cells cannot, so leucovorin rescues normal cells but not tumor cells
5-flurouracil (5FU)
-used to tx colon cancer
-combined with levamisole
5-flurouracil (5FU)
-MOA: inhibition of DNA synthesis: 5-FU converted to FdUMP which inhibits thymidylate synthetase. No dTMP formed, so no thymidine nucleotides formed = “thymidineless death”
5-flurouracil (5FU)
-what does it do?
-inhibition of RNA processing
5-flurouracil (5FU)
-leucovorin rescue?
-no leuc rescue possible
pt on chem has cough w/crackles. xr shows diffuse basilar infiltrates. DRUG?
-MOA of bleomycin (a peptide antibiotic) = fragmentation of DNA via formation of activated oxygen species (free radicals),cells accumulate in G2 w/ chromatid breaks, gaps, fragments and translocations
-little bone marrow toxicity
drug w/antiestrogenic effects for tx of breast cancer?
-used to tx brain tumors
-(they can cross the BBB)
-MOA = cross link DNA via alkylation; requires bioactivation
Which type of receptors must be present for the tx a breast cancer w/ the GnRH analogs leuprolide and goserelin?
-estrogen receptors in the tumor tissue
MOA of GnRH analogs?
MOA of GnRH analogs = act on pituitary to inhibit the release of LH and FSH, decreased LH decreases estrogen synthesis by ovaries
-cisplatin used to tx testicular and lung carcinomas
-MOA = forms intra- and interstrand cross links at N7 of guanine via hydroylsis of chloride groups = inhibits DNA replication and transcription; replacement of chloride with water forms the active drug
-S/E = nephrotoxic which is decreased by Cl- diuresis because Cl- stabilizes the
platin complex: renal toxicity causes loss of Mg++, Ca++, K+ and phosphate
-prednisone used to tx chronic lymphocytic leukemia, Hodgkin's
-MOA=apoptosis in non-dividing cells
radiation and alkylating agents
-increase tumor cell death by increasing dose
-inc tumor death by in exposure time, not the dose
-alkylating agents=moderate bone marrow depression, large doses cause severe
depression with leukopenia, thrombocytopenia and bleeding

-busulfan-skin pigmentation, pulmonary fibrosis, adrenal insufficiency
-cyclophosphamide-hemorrhagic cystitis

-cisplatin - renal damage, acoustic nerve dysfunction

-procarbazine -CNS depression

-glucorticoids=prednisone- immunosuppression, adrenal suppression, psychosis
-cytarabine - megaloblastosis

-5-fluorouracil - oral and GI ulceration

-mercaptopurine (6-MP) - toxicity potentiated by allopurinol

-methotrexate - oral and GI ulceration, bone marrow depression
-bleomycin - pulmonary fibrosis

-dactinomycin - bone marrow suppression

-doxorubicin - cardiac toxicity, bone marrow depression, red urine (not hematuria)

-etoposide - bone marrow depression
-vincristine - areflexia, peripheral neuritis, muscle weakness, paralytic ileus, alopecia

-vinblastine - loss of reflexes, bone marrow depression, alopecia

-paclitaxel (taxol) - bone marrow depression, peripheral neuropathy
-hydroxyurea - bone marrow depression

-tamoxifen - increased risk of endometrial cancer, menopausal symptoms
what is the S-phase drug that inhibit DNA pol after metabolic activation?
-cytarabine (cytosine arabinoside)
cytarabine (cytosine arabinoside)
-MOA: originally thought to inhibit DNA polymerase, but now know to inhibit DNA
synthesis by inhibiting chain elongation when AraCTP is incorporated into the growing DNA chain
Cell Cycle Specific Drugs?
-antimetabolites: cytarabine, 5FU, 6MP,6TP, methotrexate
-paclitaxel )taxol)
Cell Cycle Non-specific
-alkylating agents:mechloethamine, melphalan,CYCLOPHOSPHAMIDE, chlorambucil, busulfan,cisplatin

Cell cycle specific (phase specific)
-G1 phase
-G1 phase = 40% of cell cycle = synthesis of compounds needed to synthsize DNA
Cell cycle specific (phase specific)
-S phase
-S phase=40% of cell cycle=DNA replication and repair=antimetabolites

hydroxurea - inhibits ribonucleotide reductase

5-fluorouracil - inhibits thymidylate synthetase

6-MP, 6-TP - inhibit purine synthesis
methotrexate - inhibits DHF reductase

cytarabine - inhibits DNA chain elongation
Cell cycle specific (phase specific)
-G2 phase
-G2phase=18% of cell cycle= synthesis of molecules needed for mitosis

-bleomycin – fragmentation of DNA, cells accumulate in G2

-etoposide=stabilizes the bond between Topo II and DNA; Topo II is inhibited so
double-stranded DNA breaks remain; DNA is degraded; blocks in late S-G2
(Topoisomerases cut 1- or 2-stranded DNA to allow the strand to unwind; TOP 1 and
TOP 2 are necessary for DNA replication and RNA transcription; TOP 2 is needed for the completion of mitosis)
Cell cycle specific (phase specific)
-late G2 - early M phase
-late G2 - early M phase

-vincristine and vinblastine bind to tubulin and prevent the assembly of microtubules;cells arrest in late G2 because mitotic filaments cannot form

-However,on the USMLE these vinca alkaloids act in the M phase
Cell cycle specific (phase specific)
-M phase
-M phase = 2% of cell cycle = mitosis

-paclitaxel(taxol)–enhances polymerization of tubulin, promotes microtubule
assembly and stabilizes microtubules against depolymerization;causes mitotic arrestbecause anaphase cannot occur

-vincristine and vinblastine
Non-phase specific drugs
-can work at any step in the cell cycle, including Go

-cells are more sensitive in late G1 and S because polynucleotides are more
susceptible to alkylation in the unpaired state than in the helical form

-toxicity usually expressed when cells enter S phase and progression through cell
cycle is blocked

-Example: doxorubicin - intercalates into DNA, DNA strand scission (single and
double strand breaks) via effect on Topo II, (cells die in G2)