hypersensitivites SDL Flashcards

1
Q

discuss phase pne of type one hypersensitivity

A
  • sensitisation phase
  • allergen exposure via respiratory or skin
  • antigen presenting cells capture antigens
  • causes naive T cells to differentiate into T helper 2 cells
  • release cytokines causing B cell proliferation
  • class switch for B cells from IgM to IgE
  • type 1 = increased IgE
  • IgE binds to mast cells
  • these relocate to near where the allergen was first encountered

individual now sensitised, this phase has NO clinical signs

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2
Q

discuss phase 2 of a type 1 hypersensitivity

A
  • same allergen encountered as in phase 1
  • primed IgE coated mast cells bind to antigen of allergen
  • release of cytoplasmic granules (histamine, heparin, serotonin)
  • breakdown of mast cells
  • = pruritis, broncho-constriction and oedema
  • all occurs within 15 minutes
  • immediate hypersensitivity
  • late phase will occur within 4-24 hours and includes eosinophils seen on cytological exam
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3
Q

give 2 examples of type 1 hypersensitivity

A
  • anaphylaxis
  • atopic dermatitis in cats
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4
Q

what organs are typically effected in anaphylaxis

A

lungs typically bur liver in dogs

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5
Q

how is anaphylaxis treated

A
  • epinephrine to relax muscles
  • IV fluids
  • corticosteroids
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6
Q

how is atopic dermatitis treated as a type 1 hypersensitivity

A
  • lifestyle changes
  • glucocorticoids
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7
Q

what is a type 2 hypersensitivity

A
  • mediated by IgG antibodies circulating in blood that recognise antigens on a cell surface or in the space between cells
  • intrinsic or extrinsic antigens
  • activates classical complement pathway
  • destroys/dysfunctions cells
  • extrinsic (drug reaction) is ok
  • intrinsic (ion channels or hormone receptors) reactions are concerning
  • impacts cellular adhesion, nutrition and waste disposal
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8
Q

give example of type 2 hypersensitivites

A

myasthenia gravis
- neuromuscular disorder
- auto-antibodies against neuromuscular junction
- onset @ 6 months

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9
Q

what is a type 3 hypersensitivity

A
  • immune complex hypersensitivity
  • formation of immune complexes
  • subsequent tissue deposition
  • activation of the complement system
  • complement chemotactic for neutrophils
  • neutrophils are unable to inget the complexes that are stuck in the blood vessel walls
  • release toxic granule contents in the tissue = severe tissue damage
  • 2 subtypes: antibody excess (lots of IgG) or antigen excess (less IgG but high amounts of antigens)
  • small complexes can lead to capillary deposition leading to vasculitis
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10
Q

give 2 examples of type 3 hypersensitivities

A
  • equine recurrent airway obstruction (sensitivity to mouldy hay and dust) characterised by flared nostrils,, tachypnoea, cough and a heave line
  • canine blue eye cuased by adenovirus (excess antibody or vaccine) leading to inflammation and oedema of the cornea
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11
Q

what is type 4 hypersensitivity

A
  • cell mediated NOT antibody mediated
  • prolongd onset (24-72 hours)
  • sensitisation phase via antigen specific T cells generated
  • re-exposure = reactivation of sensitised cells which travel to site of presentation and release interferon gamma and other chemokines. macrophages are recruited, CD4+/8+ and granulopcytes
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