Hypersensitivity Reactions Flashcards
Types of Reactions
Immediate
- Type I, II, and III
Delayed
- Type IV
Type I Hypersensitivity: Overview
basic, key components, symptoms
Anaphylactic hypersensitivity
Allergic reaction
- Immediate after allergen exposure
Key components
- IgE
- Mast, basos, eos
Symptoms
- Hay fever
- Hives
- Food allergies
- Anaphylaxis
Type I Hypersensitivity: Genetics
genes, common allergens
What’s wrong with genes?
- Epithelial lining and let allergens in
- Toll like receptors incorrectly recognize normal things as DAMPs or PAMPs
- Increased IgE production, Treg defects
- Environmental factors
Common allergens: pollen, mold, food, drugs, latex
Type I Hypersensitivity: Phases
6
- APC present allergens to CD4 T
- Th2 induce IgE production to allergen
- IgE binds to FceRI reseptors on mast and basos
- Cross links nearby cell-bound IgeEs, masts and basos degranulate
- CHemical mediators released, bind to targets
- Allergy symptoms
Type I Hypersensitivity: Mediators
2
Degranulation: initial mediators, granules contain histamine and proteases
Membrane phospholipids: leukotrienes, prostaglandin are secondary mediators
- Late phase reaction
Type I Hypersensitivity: Treatments
Drug therapy
Monoclonal anti-IgE antibody
Allergy immunotherapy
Type I Hypersensitivity: Testing
In vivo skin patch
- Gold standard
- Cons: variability, severe reactions
In vitro
- Radio immuno sorbent test (RIST): while undergoing allergy immunotherapy, for total IgE
- Radio allergo sorbent test (RAST): detects allergen specific IgE
Type II Hypersensitivity:
basics, components, effecs
Antibody mediated cytotoxic hypersensitivity
Key components
- IgG, IgM against cell surface antigen
Effects
- Cell destructuin
- Inhibition/increase in cell function
Type II Hypersensitivity: Examples
Transfusion reactions
Hemolytic disease of the newborn
AI hemolytic anemia
Goodpasture’s syndrome
Hashimoto’s syndrome
Type II Hypersensitivity: Coomb’s Test
direct vs indirect
Direct
- Need baby blood, detects in vivo
Indirect
- Need mom serum, detects ex vivo binding
Followed by anti-IgG or anti-C3b to determine if IgG or IgM
Type III Hypersensitivity: Overview
key components and process
Complex-mediated hypersensitivity
Key components
- IgG, IgM
Process: ag-ab complex precipitate into tissue, macros and pmns migrate to affected areas, lysosome enzyme releases, tissue damage
Type III Hypersensitivity: Symptoms
2
Arthus reaction: localized redness, edema, 3-8 hour peak
Serum sickness
Generalized type 3 reaction
- Passive immunizations of humans with animal proteins, makes ABs against foreign animal proteins
- Immune complexes form + deposit in tissue
- Symptoms: headache, fever, joint pain, lymphadenopathy
Type III Hypersensitivity: Testing and Conditions
Tests: ANAs, flourescence, anti-IgG, rheumatoid factor, complement testing
Conditions: lupus, RA, bee stings, drugs, post strep glomer.
Type IV Hypersensitivity: Basics
key components, processes
Cell-mediated or delayed type
Key components
- Th1 cells, macros
Process
1. APC present antigen to Th -> turin into Th1
2. They release cytokines, macros come, induce inflammation
3. CD8T destroy target cells
Type IV Hypersensitivity: Conditions
Intracellular pathogens: leprosy, leishmaniasis, herpes, TB
Contact dermatitis: low molecular weight compounds bind to protein through skin, sensitize Th1, induces inflammation
Hypersensitivity pneumonitis: from bacteria, fungal spores
