Phase II Metabolism

  1. UGT aka
    UDP-Glucuronosyltransferase
  2. UGT transfers ___________ to substrate
    β-D-glucuronide
  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
    UGT2B7
  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)?
    Hyperbilirubinemia
  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?
    Hypercarnivore
  15. Due to hypercarnivorous characteristic of house cats, they have lost _______ enzyme.
    UGT1A6
  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?
    Sulfotransferases
  18. Sulfotransferases are responsible for biotransfering what anticoagulant drug?
    heparin
  19. ________ SULTs are located in the Golgi.
    Membrane bound
  20. ________ SULTs are mainly responsible for biotransfering sulfonate xenobiotics, bile acids.
    Cytosolic
  21. What subfamily of GST is responsible for metabolism of inflammatory agents such as protaglandins.
    Microsomal
  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
    GSTT1*0
  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.
    GST
  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?
    Hydralazine
  29. Inactivation of neurotransmittors is associated with what enzyme?
    COMT
  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
Author
HUSOP2014
ID
216876
Card Set
Phase II Metabolism
Description
Phase II Metabolism
Updated