Allergy and asthma Flashcards
Why do we get hypersensitivity?
-consequence of immunological arms race with pathogens
What is hypersensitivity?
-where the immune response contributes to disease
type 1 hypersensitivity: IgE antibody
- atopic asthma
- hay fever (allergic rhinitis)
IgG tissue self-antigen
goodpasture’s syndrome
IgG soluble self-antigen
Systematic Lupus Erythematosus (SLE)
activated macrophages
pulmonary tuberculosis
Diagnosis of IgE allergen sensitivity: Immediate allergen skin prick test responses (10 mins)
Diameter of the raised blanched weal identifies • the profile of allergen sensitivity
• the IgE antibody titre
mast cells (mucosal tissue) and basophils (blood)
Mast cells bind IgE to form a functional response unit to allergens/parasites
activation of degranulation of mast cells by IgE
Release of • Histamine • Chemokines • Cytokines • Leukotrienes • Prostaglandins • Growth factors
Asthma Histology
- inhaled allergens cause inflammation
- mast cell degranulation
- smooth muscle contraction (wheeze)
- airway remodelling-lumen greatly reduced
- sub-epithelial collagen is thicker
- epithelium is more abundant, along with mucus
Asthma
The interstitium (tissue around the bronchiole) has more inflammatory cells (those with pink cytoplasm = eosinophils
Eosinophils
- gram stain pink by eosin dye
- IgG and IgE antibody bind to parasite
- eosinophils bind to IgG/IgE on parasite
- release of granule contents on parasite membrane
i. e. Major Basic Protein (MBP) - toxic for parasites
Type 2 hypersensitivity example 1: Hashimoto’s Thyroiditis
-Auto-antibody to thyroid protein (thyroglobulin)
Thyroid
-thyroxine - replacement therapy
Type 2 hypersensitivity example 2: Sjogrens Syndrome
- parotid enlargement
- auto-antibodies to antigen* in the glands that produce tears and saliva
Type 2 hypersensitivity: Auto-immune haemolytic anaemia
-acquired autoimmune disease