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2013-10-20 12:26:38
biochem presentations

biochem presentations
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  1. Basophils
    granulocytes that release chemicals to promote inflammation
  2. Eosinophils
    granulocytes that are cytotoxic killers that primarily target parasites
  3. Neutrophils
    phagocytic granulocytes that ingest and kill bacteria
  4. Monocytes/Macrophages
    Antigen presenting cells that ingest pathogens and activate helper T-cells
  5. B-lymphocytes
    Antigen specific cells that have not come into contact with their antigen
  6. Plasma cells
    Activated B-lymphocytes that have been in contact with their antigen, and produce specific antibodies
  7. Memory B-cells
    cells that have been in contact with their antigen, and are in circulation to fight secondary exposure
  8. Helper T cells
    lymphocytes that release cytokines to help activate B-lymphocytes
  9. Cytotoxic T-cells
    lymphocytes that kill self cells carrying foreign antigens by inducing apoptosis
  10. Natural Killer cells
    lymphocytes that target abnormal self cells and induce apoptosis
  11. Warfarin
    Inhibits vitamin K epoxide reductase
  12. Heparin
    promotes endogenous anti-thrombin activity
  13. Dabigatran
    Direct thrombin inhibitor
  14. Apixaban
    Factor Xa inhibitor
  15. Sirolimus
    • Derivative of Rapamycin
    • Immunosuppresent for organ transplants
    • Acts on T and B cells by binding FKBP, which forms immunosuppressive complex inhibiting mTOR activity (mammalian target of rapamycin)

    Binding mTOR inhibits cell proliferation/synthesis
  16. Glycogen synthase
    Extends glycogen chains (a-1,4-glycosidic bonds)
  17. Glycogen phosphorylase
    breaks glycogen chains (a-1,4-glycosidic linkages)
  18. Glycogen branching enzyme
    transfers 7 linked glucose residues to the next chain (a-1,6-glycosidic linkage)
  19. Glycogen debranching enzyme
    transfers 3 residues to another chain (a-1,6-glycosidic chain)
  20. Type 0 GSD
    deficiency in glycogen synthase
  21. Type 1 GSD
    • most common: 
    • deficiency in glucose-6-phosphatase or G6P transporter
  22. Type 2 GSD
    alpha-1,4-glycosidase deficiency in heart+ lysosomes
  23. Type 3 GSD
    inherited: build up of glycogen due to glycogen debranching enzyme deficiency
  24. Type 4 GSD
    buildup of glycogen due to glycogen branching enzyme deficiency
  25. GSD Type 5
    Deficiency of myophosphorylase (cant break glycogen in muscle)
  26. GSD type 6
    deficiency in liver glycogen phosphorylase (leads to liver enlargement)
  27. GSD type 7
    Deficiency in phosphofructokinase in muscles-> inability to use glycogen leads to muscle breakdown for energy.
  28. Name 3 of the most common drugs that induce agranulocytosis
    Clozapine, Dapsone, Aminopyrine
  29. Agranulyctosis
    • Direct or immune mediated toxicities
    • Treatment based on neutrophil recovery.
  30. Arsenate poisoning
    symptoms: headache, drowsiness, fingernail pigmentation change

    • Arsenite (3+): binds GSH, inhibits pyruvate dehydrogenase
    • Arsenate (5+): binds where phosphate usually binds. inhibits glycolysis

    Can be treated with dermercaptusuccinic acid (DMSA)