Phase II Metabolism

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  1. UGT aka
  2. UGT transfers ___________ to substrate
  3. What is UDPGA and what isoforms utilize it?
    • Uridine-5-diphosphate-a-D-glucuronic acid
    • UGT1, UGT2A and UGT2B
  4. What are UGT GI forms? What are they important for?
    • UGT1A7, 1A8, 1A10
    • 1st pass metabolism and affects bioavailability
  5. ___________ is the major enzyme for codeine glucuronidation
  6. What disease is associated with mutation of UGT1A1 gene?
    Crigler-Najjar syndrome
  7. Mutation in UGT1A1 gene will cause what biological effect(ie.HTN is a biological effect)?
  8. UGT1A1 mutation causes __________ which produces ___________ in the serum.
    • Crigler-Najjar syndrome
    • High bilirubin
  9. Mutation in UGT1A1 (increase/decrease) in glucuronidation acivity that leads to ____ and ___?
    • decrease
    • congenital nonhemolytic jaundice
    • unconjugated hyperbilirubinemia
  10. UGT1A1*28 allege mutation is associated with what disease?
    Glibert Syndrome
  11. Glibert syndrome causes __________ in blood serum due to mutation in _________ allele.
    • increase in unconjugated bilirubin
    • UGT1A1*28
  12. Glibert syndrom is a mutation in what region of the gene?
    TATA box
  13. Treating UGT1A1*28 mutation with _______ drug leads to severe delayed diarrhea and _________.
    • Irinotecan
    • neutropenia
  14. House cats have lots their ability to glucuronidate certain agents due to what characteristic?
  15. Due to hypercarnivorous characteristic of house cats, they have lost _______ enzyme.
  16. Loss of _________, cats can not glucuronidate ___&___ due to its increase in toxicity and slow clearance.
    • UGT1A6
    • APAP & acetysalicylic acid
  17. During fetal development, __________ is the enzyme that is responsible for biotransformation of retinol?
  18. Sulfotransferases are responsible for biotransfering what anticoagulant drug?
  19. ________ SULTs are located in the Golgi.
    Membrane bound
  20. ________ SULTs are mainly responsible for biotransfering sulfonate xenobiotics, bile acids.
  21. What subfamily of GST is responsible for metabolism of inflammatory agents such as protaglandins.
  22. Which isoform of GST causes a null mutation that leads to colon cancer.
    Null mutation (GSTM1*0)
  23. Which null mutation of GST subfamily leads to increase in chemotherapy side effects
  24. Increase in incidence of asthma is associated with what polymorphism?
    Null GST polymorphism
  25. Overexpression ___________ leads to increase in resistance to nitrogen mustards binding to DNA.
  26. ______&______ isoforms of are known as fast acetylators which is responsible for ________ drug used for tuberculosis.
    • NAT2*12 and NAT2*13
    • Isoniazid
  27. Slow acetylators can do lead to what when hydralazine is given?
    tachycardia or hypotension
  28. Poor metabolism of what drug by NAT lead to severe cadiogenic effects?
  29. Inactivation of neurotransmittors is associated with what enzyme?
  30. Polymorphisms in the enzyme resposible for metabolizing neurotransmittor can lead to what disease. (Name one)
    • Schizophrenia
    • Parkinson's
    • alcoholism
  31. What enzyme metabolizes antineoplastic and immunosupressive agents?
    Thiopurine S-methyltransfersase
  32. activation of _______ drug by ___________ into 6-MP.
    • Azathiprine
    • Glutathione S-transferase
  33. 6-MP is metabolized by ___________.
    Thiopurine S-methyltransferase
  34. Polymorphisms in TPMT leads to what severe pathophysiologic effect, due to increased concentration of drug that are metabolized by TPMT.(Name one)
    • Hepatotoxicity
    • life-threatening myelosuppression
Card Set:
Phase II Metabolism
2013-05-01 05:12:33
HUSOP GEN Final Exam

Phase II Metabolism
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