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
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
3
Q
give 2 examples of type 1 hypersensitivity
A
- anaphylaxis
- atopic dermatitis in cats
4
Q
what organs are typically effected in anaphylaxis
A
lungs typically bur liver in dogs
5
Q
how is anaphylaxis treated
A
- epinephrine to relax muscles
- IV fluids
- corticosteroids
6
Q
how is atopic dermatitis treated as a type 1 hypersensitivity
A
- lifestyle changes
- glucocorticoids
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
8
Q
give example of type 2 hypersensitivites
A
myasthenia gravis
- neuromuscular disorder
- auto-antibodies against neuromuscular junction
- onset @ 6 months
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
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
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