drugs and immune system.txt

  1. which immunisations are live attenuated and who can they not be given to?
    • BCG
    • Oral polio
    • Yellow fever
    • MMR
    • not to immunocompromised as they are active organisms
  2. which immunisations are neutralised toxins i.e. PASSIVE
    • diphtheria
    • botulism
  3. give 3 examples of dead organisms or extracts (active)
    • hep a and b
    • HiB (haemophilus influenzae b)
    • influenza
    • pneomococcus
  4. what are the effects of steroids? 2 main categories
    • anti inflammatory
    • immunosuppressive
  5. how do steroids reduce inflammation?
    • reduce production of PG, LT, thromboxane, PAF so
    • reduced vasodilation
    • reduced cap perm so less oedema
    • reduced leukocyte infiltraion
    • reduce bronchoconstriction
    • reduce pain
    • reduce histamine release from basophils
  6. what is the mechanism of action of steroids?
    • bind to intracellular glucocorticoid and mineraocorticoid receptors and also bind to cell surface receptors
    • regulate gene transciption and expression
    • e.g. makes lipocortin a phospholipid binding protein which inhibits phospholipoase A2 from converting PL to AA so less PG and PAF made
  7. how long does it take before anti inflame of steroids start? and why?
    4-6 hours because DNA and protein synthesis is involved
  8. what are the side effects of steroids?
    • iatrogenic cushing's syndrome: BUT NO HIRSUTISM!
    • due to negative feedback, reduce hypothalamic and pituitary drive to make cortisol and aldosterone so if stop steroids abruptly can get iatrogenic addison's disease as adrenals have atrophied
    • mineralocorticoid effects: salt and water retention - hypertension; hypokalaemia; alkalosis
    • immune suppression due to thymus involution
    • osteoporosis due to increased bone catabolism so inc Ca conc
    • decreased wound healing
    • easy bruising
    • due to reduced collagen formation and fibroblast proliferation and inc protein catab
    • carbohydrate metabolism: less glucose uptake and use and increase gluconeogenesis so hyperglycaemia and diabetes
    • increased protein catabolism: reduced muscle bulk, wound heal, bruise, thin skin, cardiomyopathy and myopathy
    • fats: redistribution of fat with moon face, buffalo hump, supraclavicular fat pads, central adiposity, thin limbs. increased HSL hormone sensitive lipase expression so increased free fatty acids
    • CNS: depression and psychosis
  9. What is cyclosporin derived from?
    fungus norway
  10. what is the mechanism of action of cyclosporin?
    it binds cyclophilin in T cells and inhibits calcineurin to reduce IL2 transcription
  11. give 2 uses of cyclosporin?
    • anti rejection treatment for transplant
    • 2nd line for autoimmune diseases
  12. what are the side effects of cyclosporin
    • increased urea and creatinine
    • hypertension
    • hirsutism
    • gum hypertrophy
    • peptic ulcer
    • bit of BM depression
    • narrow TI so needs TDM (therapeutic drug monitoring)
    • interacts with hepatic enzyme inducers and inhibitors e.g. ERYTHROMYCIN inhibits cytochrome p450 system so less metabolism of ciclosporin therefore increased toxicity
  13. What is tacrolimus made by?
  14. what is the MOA of tacrolimus?
    post T cell receptor activation inhibition of calcineurin so reduced IL2 and other cytokine production
  15. what is tacrolimus used for?
    to reduce acute renal allograft rejection
  16. whats the difference between tacrolimus and cyclosporin?
    • tacrolimus is more potent
    • and therefore also more toxic and more immunosuppressive so causes more opportunistic infections
  17. what type of drug is azathioprine?
    • purine anti metabolite
    • prodrug activated to 6 mercaptopurine
  18. what is the MOA of azathioprine?
    • aza is converted to a fraudulent purine analogue
    • inhibits DNA synthesis so reduces proliferation of WBC esp B and T lymphochytes
  19. what is azathioprine used for? 2 main categories and give subcategories
    • transplant - reduce rejection
    • autoimmune diseases such as RA, IBD, AIH, MS, pemphigus (skin sores and blisters)
  20. how is azathioprine metabolised?
    xanthine oxidase
  21. what drug can increase the toxicity of azathioprine and how?
    allopurinol can as it inhibits xanthine oxidase, so less aza is metabolised
  22. what are the side effects of azathioprine?
    • BM toxicity
    • increased risk tumour especially lymphoma (NHL) and SCC
    • increase risk infection, pancreatitis
    • anorexia, N and V
  23. what type of drug is cyclophosphamide?
    nitrogen mustard alkylating agent
  24. what is the MOA of cyclophosphamide?
    crosslinks DNA and prevents replication
  25. what is cyclophosphamide especially useful for?
    B cell suppression
  26. give 3 main uses of cyclophosphamide?
    • lymphoma
    • BM transplantation
    • autoimmune diseases
  27. give 3 main SE of cyclophosphamide
    • haemorrhagic cystitis
    • pancytopenia - so anaemia, neutropenia so inc infection, thrombocytopenia so bleed
    • cardiotoxicity
  28. what type of drug is mycophenolate mofetil? and how does it work?
    purine anti metabolite to reduce lymphocyte production by reducing DNA synthesis
  29. when is mycophenolate mofetil used?
    • alternative to azathioprine, if aza toxicity
    • only use: PREVENT TRANSPLANT REJECTION - immunosuppression
  30. in which ways is mycophenolate mofetil better than azathioprine?
    • more specific inhibition of lymphocytes than azathioprine
    • less BM toxicity
    • less infection
  31. what are the SE of mycophenolate mofetil?
    • BM toxicity
    • tumour development
  32. what type of drug is methotrexate?
    anti folate drug
  33. what is the MOA of methotrexate?
    inhibits dihydrofolate reductase to reduce RNA and DNA synthesis
  34. give 5 uses of methotrexate
    • RA
    • Ank spond
    • Crohns
    • Psoriatic arthritis
    • ALL
  35. what must you give with methotrexate?
    folate supplements
  36. how often is methotrexate given?
    once a week, orally
  37. what are the side effects of methotrexate? 4
    • BM suppression: anaemia, neutropenia
    • hepatitis
    • teratogenic
  38. give 2 types of antiTNFa
    • etanercept: receptor blocker
    • adalimumab or infliximab: MAb to TNFa
  39. what is antiTNFa used for?
    DMARD resistant RA, Ank spond, severe Crohns
  40. what is INF1B used for?
    MS - reduce relapse
  41. What is INF1a used for?
    in CHRONIC hep B and C to prevent further hepatic damage
  42. what is the MOA of thalidomide?
    inhibits TNF synthesis
  43. what is the use of thalidomide?
    • multiple myeloma
    • leprosy
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drugs and immune system.txt