Week 1.5 Flashcards
What are the 2 stages in all hypersensitivity reactions
Sensitisation stage
Effector stage
Features of type 1 hypersensitivity reaction
Immediate reaction - symptoms onset minutes up to Hours
IgE mediated
Mechanism of type 1 hypersensitivity reaction
- On first exposure to allergen, B cells produce IgE antibodies
- Some remaining IgE antibodies bind to Fc receptors of mast cells
- Mast cells circulate the blood stream
- On re-exposure to the allergen, the antigen binds onto IgE on mast cells causing mast cells to degranulate
- Mast cells release histamine and inflammatory cytokines
Common allergens causing type 1 hypersensitivity
Pollen
Food
Animals
Drugs
Symptoms that can be caused by type 1 hypersensitivity
Urticaria - very itchy lesions that look like hives
Angioedema
Anaphylaxis (if severe reaction)
Asthma
Symptoms of anaphylaxis
Laryngeal / pharyngeal oedema
Bronchospasm
tachypnea
Hypotension
Tachycardia
Urticaria
Allergic rhinitis / conjunctivitis
Investigations for type 1 hypersensitivity
History
Skin prick test
Challenge test if skin prick test is negative but history strongly suggests so
First line treatment for type 1 hypersensitivity
Avoid allergen
Management for acute T1 hypersensitivity attack
- Anti-histamines
- Corticosteroids
- Epi pen (adrenaline pen) if anaphylaxis
Examples of anti-histamines
Chlorphenamine
Diphenhydramine
Examples of corticosteroids used in type 1 hypersensitivity
Prednisolone
Features of type 2 hypersensitivity
Takes hours - days for reaction after exposure
IgG and IgM mediated
Cytotoxic reaction
How does IgG and IgM cause cytotoxic reaction in type 2 hypersensitivity
Activation of complement system
Antibody dependent cell mediated cytotoxicity (ADCC)
Opsonization
Describe the antibody-dependent cell mediated cytotoxicity in type 2 hypersensitivity
- IgG/IgM binds to antigens
2 Natural killer cells bind to the Fc portion of IgM/IgG antigen complexes - NK cells causes cell death
Examples of conditions due to Type 2 hypersensitivity
Haemolytic anaemia
Goodpasture’s syndrome
Grave’s disease
Bullous pemphigoid
What is Goodpasture’s syndrome
When the IgG and IgM antibodies are directed to attack a specific collagen found in basement membrane of alveoli and glomeruli
Causes lungs and kidney damage
Presentation of Goodpasture’s syndrome
Haemoptysis
SOB
Renal dysfunction - decreased urine output
Renal failure
Features of type 3 hypersensitivity
Takes hours - days for reaction to occur after exposure
Antigen-antibody immune complex mediated
Difference between type 2 and type 3 hypersensitivity
In type 3, the antibodies are bound to soluble antigens unlike in type 2 where IgG and IgM are bound to antigens on cells
In type 3, it triggers inflammation cascade in certain areas instead of cytotoxicity in type 2
Mechanism of type 3 hypersensitivity
- sensitisation
- effector stage: Antibody covers the soluble antigen forming antibody-antigen complexes. The complexes can move and deposit in certain areas and trigger inflammation there
The immune complexes in type 3 hypersensitivity often deposit in
Blood vessels
Synovial joints
Glomerular basement membrane
Examples of conditions due to type 3 hypersensitivity
Rheumatoid arthritis
SLE
Post streptococcal glomerulonephritis
Features of type 4 hypersensitivity
Takes days for reaction to occur after exposure
T cell mediated
Why is type 4 hypersensitivity called delayed hypersensitivity
Because it takes time for T cells to recruit to sites where antigen is at hence causes delayed response