L11 Hypersensitivity Flashcards
What is secreted by plasma cells in type I hypersensitivity reaction?
IgM
Who recognises antigen for the first time in type IV hypersensitivity reaction?
Dendritic cells
How is type I hypersensitivity reaction triggered?
By the binding of antigen to the antibody bound to mast cell in individuals who are previously sensitised. Mast cell will then degranulate.
Type I hypersensitivity MOA
First exposure
1. Sensitization (T-helper and B cells)
2. IgE production
3. Arming of mast cells with IgE
Second exposure
1.Binding of antigen to IgE antibody on mast cell
2. Release of chemokines by mast cells
3. Inflammation
What are the clinical effects of the release of Mb phospholipids (leukotrienees and PGs) in type I hypersensitivity reactions?
- Decrease in blood pressure (vasodilation)
- Mucus secretion
- Smooth muscle contraction (bronchospasm)
What are the clinical effects of the release of histamines in type I hypersensitivity reactions?
- Decrease in BP (vasodilation)
- Smooth muscle constriction (bronchospasm)
- Localised swelling
What is used to counteract the systemic effect of anaphylactic shock?
Adrenaline (epinephrine) –> vasoconstriction (opposing the generalised vasodilation)
How are injuries caused in type II hypersensitivity reaction?
- Phagocytosis (opsonization via antibody)
- Inflammation (complement activation)
- Cellular dysfunction (myasthenia gravis and graves disease)
What instances is type II hypersensitivity common in?
- Transplant rejection
- Blood transfusion mismatch
What is the common clinical sequelae of type III hypersensitivity reactions?
Fibrinoid necrosis at blood vessels, kidney and joints
What are the 2 main hypersensitivity reaction in transplant rejection
II and IV
What are the 2 main hypersensitivity reaction in dental surgery
I and IV
