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5 Written questions

5 Matching questions

  1. Anti neoplastics
  2. Anti Leukemics
  3. Effects of Allopurinol Tx on LNS pts
  4. Folate antagonists as Antibiotics, Trimethoprim
  5. Why allopurinal decreases rate of purine biosynthesis
  1. a is a selective inhibitor of bacterial DHFR, and is often administered with sulfamethoxazole, an inhibitor of THF biosynthesis from folic acid

    This works because folic acid is biosynthesized in bacteria, but is a component of diet in humans
  2. b Reduces urate in LNS pts by blocking xanthine oxidase rxns

    Ineffective in reducing rate of de novo purine biosynthesis, since it cannot synthesize allopurinol ribonucleotide from allopurinal and PRPP, it requires HGPRT

    Can have neurological effects due to the brains reliace on salvage pathways for most purine nucleotide production and needs GTP for dopamine formation
  3. c It lowers the PRPP pool by binding and using HGPRT to form an allopurinol ribonucleotide

    This inhibits the action of glutamine PRPP amidotransferase

    and Thus there is less flux through the de novo purine pathway
  4. d 6 mercaptopurine
    6 thiaguanine
    These compounds compete with hypoxanthine and guanine for the salvage enzyme HGPRT.
    They are converted by HGPRT into respective ribonucleotides, they inhibit the committed step of de novo purine biosynthesis pathway catalyzed by Gln PRPP amidotransferase, an effect similar to allopurinol
    They are also incorporated into DNA and RNA
  5. e some discussed earlier
    araC, triphosphate interferes with DNA synthesis

5 Multiple choice questions

  1. it is similar to dUMP and acts as a suicide inhibitor or thymidylate synthetase TS. This kill rapidly dividing cells Tumors and immune cells
  2. ammonia toxicity
    Ornithine transcarbamoylase def
    in both cases carbamoyl P accumulated in liver mitochondria, which enters cytoplasm, which drives overproduction of orotate via the pyrimidine biosynthesis pathway.
  3. serum urate decraeases
    serum hypoxanthine and xanthine increase, these are more soluble and easily excreted
    Decreases total rate of purine biosynthesis
  4. Familial Orotic Aciduria are inherited deficincies in orotate phosphoribosyltrandferase OPRT and or OMP decarboxylase

    These slow the formation of OMP from orotate, and UMP from OMP.

    Signs and symptomes are growth retardation, megaloblastic anemia, crystalline orotate in urine

    Tx effectively by large doses of orally administered uridine
  5. ADA deficiency causes abnormal build up of Deoxyadenosine containing nucleotides including dATP

    dATP feedback inhibits ribonucleotide reductase, allosterically choking off production of other dNTPs

    Lack of dNTPs prevents DNA synthesis preventing proliferation of lymphocytes.

5 True/False questions

  1. Purine Nucleosid Phosphorylase PNP deficiencyanother rare cause of SCIDS Disorder, since Ino, dIno, Guo and dGuo are strong subtrates of PNP and Ado and dAdo is weak we get a larger build up of dAdo relative to dNTPs


  2. Second Step in Pyrimidine biosynth ATCaseusing Carbamoyl phosphate synthetase II, CPS II takes CO2 and Glutamine to Carbamoyl phosphate using 2 ATP

    In mitochondria CPS I uses NH4+ as a nitrogen source, this is part of the urea cycle


  3. Anti virals, Acyclovir, AraAAZT, DDC, ddI
    Used to treat HIV and AIDS
    Triphosphates inhibit retroviral reverse transcriptase


  4. Other drugs related to nucleotides and nucleotide metabolismUses Ribonucleotide Reductase to take A,G,C,UDP to dA,dG,dC,dUDP

    All can form to triphosphate form easily

    Formation of dTMP and dTTP requires Thymidylate Synthetase, which is dependent on THF cycle and dihydrofolate reductase.


  5. Severe Combined Immunodeficiency SyndromeSCIDS is an Adenosine Deaminase ADA deficiency

    boy in the bubble syndrome, failure of both B and T lymphocytes to proliferate

    all forms inherited, half result from absence of ADA encoded on chromosome 20

    First target for human gene therapy