PHRD5015 Lecture 17 (Ju) - Hypersensitivity Reactions

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PHRD5015 Lecture 17 (Ju) - Hypersensitivity Reactions
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2013-10-30 07:38:26
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PHRD5015 Hypersensitivity Reactions
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Hypersensitivity Reactions
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  1. hypersensitivity reaction
    unwanted immune response against endogenous/innocuous foreign Ags that produce tissue damage
  2. IgE-mediated immediate rxn
    Type I hypersensitivity
  3. antibody-mediated cytotoxic rxn
    Type II hypersensitivity
  4. hypersensitivity rxn cause by Ab-Ag immune complex
    Type III hypersensitivity
  5. T cell-mediated delayed-type hypersensitivity rxns
    Type IV hypersensitivity
  6. sensitization
    • first step of Type I rxn
    • upon initial exposure to Ag, B cells are activated to produce IgE Ab's
    • clinically silent
  7. role of mast cells (and basophils) in Type I hypersensitivity
    their high affinity FcR's bind IgE & allow for recognition upon re-exposure -> IgE crosslinking activates mast cells to degranulate
  8. 4 stages of Type I rxn
    • 1) sensitization
    • 2) mast-cell binding
    • 3) Ag challenge
    • 4) degranulation
  9. 4 types of mast cell-released mediators & fcn
    • 1) proteases - tissue destruction
    • 2) amines (histamine) - vasodilation, SM contraction
    • 3) lipid mediators - bronchoconstriction, vascular permeability
    • 4) cytokines/chemokines - Th2 response, mast cell proliferation, inflammation
  10. mast cell origin, location, allergy role
    • 1) bone marrow (myeloid)
    • 2) near blood vessels/not in circulation
    • 3) activate eos to express FcRI
  11. basophil origin, location
    • 1) bone marrow (myeloid)
    • 2) in circulation
  12. 3 steps as targets for Type I rxn treatment
    • 1) Th2 differentiation & IL-4/13 release
    • 2) IgE production & binding to mast cells
    • 3) inflammation induced by mast cell mediators
  13. method to inhibit Th2 differentiation/IL release
    • Th1 stimulation
    • inject pt with increasing doses of allergen -> diversion of IgE-dominated Th2 response to Th1
  14. 2 methods to inhibit IgE production/binding to mast cells
    • 1) anti-IgE Ab's (Xolair)
    • 2) IgE Fc constructs to occupy FcRI
  15. method to inhibit inflammation induced by mast cell mediators
    block eosinophil recruitment/activation by neutralizing CCR3 & IL-5
  16. treat bronchoconstriction in asthma
    2-adrenergic receptor agonists
  17. 5 methods to treat asthma
    • 1) leukotriene modifiers (inhibit airway constriction)
    • 2) adenylyl cyclase activators (relax bronchial SM)
    • 3) p-diesterase inhibitors (increase cAMP)
    • 4) corticosteroids (anti-inflammatory)
    • 5) mast cell inhibition (inhibit degranulation)
  18. mechanism of Type II rxn
    IgG/IgM recognizes/binds Ag -> complement activated -> opsonization activates phagocytic cells to produce pro-inflammatory cytokines -> inflammation/tissue injury
  19. ADCC
    • antibody dependent cell-mediated cytotoxity
    • Type II rxn
  20. hyperacute graft rejection
    • Type II rxn
    • ABO Ag on graft
    • affects kidney/heart
  21. Goodpasture's syndrome
    • Type II rxn
    • affects kidneys, lungs
  22. immune mediated hemolytic anemia
    • Type II rxn
    • affects blood
  23. myasthenia gravis
    • Type II rxn
    • affects muscle
  24. Grave's disease
    • Type II rxn
    • affects thyroid
  25. insulin resistant diabetes
    • Type II rxn
    • affects insulin receptor
  26. mechanism of Type III rxn
    IgG/IgM recognizes/binds Ag -> complex is >1000kDa & gets stuck in blood vessel walls -> complement activated -> opsonization activates phagocytic cells to produce pro-inflammatory cytokines -> systemic inflammation/tissue injury

    **SIMILAR TO TYPE II, BUT IMMUNE COMPLEX MEDIATED**
  27. systemic lupus erythematosus
    • Type III rxn
    • Ag's are self-DNA or nucleoproteins; deposits in small arteries
  28. DTH
    • delayed type hypersensitivity rxn 
    • Type IV rxn
  29. mechanism of Type IV rxn
    • Stage 1 (Sensitization): Ag taken up by APCs that activate memory T cells; memory T cells circulate (3-10 days)
    • Stage 2 (Elicitation): re-exposure attracts memory T cells to site; macrophage recruitment, IFN, IL-3, GM-CSF, TNF secretion (24-48hr)
  30. 3 examples of Type IV rxn
    • 1) insulin dependent DM
    • 2) MS
    • 3) RA
  31. ADR to penicillin
    anaphylaxis
  32. ADR to halothane
    hepatitis
  33. ADR to clozapine
    agranulocytosis (neutropenia)
  34. ADR to procainamide
    lupus
  35. hapten
    low molecular weight chemical that is not immunogenic themselves, but upon binding to endogenous proteins & forming a complex is large enough to elicit an immune response
  36. drugs that cause agranulocytosis (6)
    • 1) clozapine
    • 2) aminopyrine
    • 3) amodiaquine
    • 4) propylthiouracil
    • 5) sulfamethoxazole
    • 6) carbamazepine
  37. drugs that cause hepatoxicity (4)
    • 1) troglitazone
    • 2) halothane
    • 3) tienilic acid
    • 4) diclofenac
  38. 2 most devastating drug-induced cutaneous rxns
    • Stevens-Johnson syndrome
    • Toxic epidermal necrolysis
  39. drugs most frequently involved in severe cutaneous rxns (5)
    • 1) sulfamethoxazole/trimethoprim
    • 2) nevirapine
    • 3) carbamazepine
    • 4) phenytoin
    • 5) lamotrigine
  40. most common Type I hypersensitivities (2)
    • 1) allergic rhinitis
    • 2) asthma
  41. Type II rxn involves what type of Ag
    cell-surface or matrix-assoc'd
  42. reactant for Type III rxns
    IgG or IgM
  43. granulocyte responsible for activating inflammation in Type III rxns
    neutrophils
  44. propensity of an individual to produce IgE Ab's in response to various environmental Ag's & develop strong Type I immediate hypersensitivity reactions
    atopy
  45. 3 genetic factors contributing to atopy
    • 1) genes that affect IgE responses
    • 2) genes that encode for HLA class II molecules
    • 3) genes that affect clinical responses to tx's
  46. 2 general treatments of allergy
    • 1) immune modulation
    • 2) blockade of effector pathways
  47. Type A ADR
    • "augmented"
    • can be predicted, alleviated by dose reduction
  48. Type B ADR
    • idiosyncratic
    • unexpected/undocumented rxn
  49. 3 most common targets of drug-induced hypersensitivity
    • 1) liver
    • 2) skin
    • 3) blood

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