L:22 Hypersensitivity disorders Flashcards
What is hypersensitivity
Exaggerated immune response harmful to organism itself
Classifications of the 4 types of hypersensitivity reactions
Antibody-mediated
Cell-mediated
Antibody mediated effector mechanisms
Type I, II, and III
Correspond to defenses against extracellular pathogens
Cell-mediated effector mechanisms
Type IV- corresponds to defense against intracellular pathogens
Clinical manifestation of Type I hypersensitivity caused by?
Mediators secreted by Mast cells
What type of hypersensitivity takes place when antibodies specific for the cell and tissue Ags cause injury or disease to the tissue?
Type II
What is it called when Abs bind to circulating Ags to form immune complexes, which deposit in vessels, leading to inflammation in the vessel walls (vasculitis)
Immune Complex diseases (type III hypersensitivity)
What is the cause of type IV hypersensitivity?
T cell mediated disease caused by inflammation caused by cytokines produced by CD4 Th1 and Th17, or killing of host by CD8 CTLs
Individuals with a strong propensity to develop allergic reaction is said to be what?
Atopic
Type I hypersensitivity rxn is controlled by the binding of what?
IgE Abs to FcĘR1 located on the membrane of MAST CELLS, BASOPHILS and EOSINOPHILS
Most IgE produced following initial contact with Ag becomes?
Fixed on the surface of mast cell and basophils..
Second contact with Ag, the Ag-Ab rxn occurs predominantly on mast cell and basophil membrane
Hallmarks of Immediate hypersensitivity
Acute vascular, smooth muscle reactions, and inflammation
What causes vascular dilation
Prostaglandins
Histamines
What causes prolonged smooth muscle contractions?
Leukotrienes
What induces local inflammation (the late phase rxn)
Cytokines
Time frame of immediate and late phase rxn
Immediate vascular and smooth muscle develops within minutes.
The late-phase rxn develops 2-4 hrs. later characterized by inflammation
reversible airway obstruction often caused by inflammatory mediators from mast cells
Asthma
*spasmatic contraction of smooth muscle surrounding bronchi decreasing lumen size and causing SOB
Anaphylaxis
Rapid release of vaso active amines from mast cells and basophils as well as cytokines. Results in smooth muscle contraction in vasculature and vasodilation of capillary epithelium. **BP decreases leading to vascular shock* contraction of smooth muscles in bronchi cause difficulty breathing
In type II hypersensitivity IgG and IgM activate what pathways?
Complement system by classical pathway. results in byproducts that recruit leukocytes to induce inflammation
Type II
What activates leukocytes resulting in pro-inflammatory response?
IgG antibodies binding to neutrophil and macrophage Fc receptors.
Reactive oxygen and lysosomal enzymes are released and damage adjacent tissue because Ab-Ag complexes are formed on target cell
Type III
Ab-Ag complexes deposit where?
blood vessels and other sites resulting in vascular inflammation, and subsequent ischemic damage to tissue
Type III
Major mechanism triggering tissue damage
Classical activation of complement
Type III
Tissue damage is mediated by?
- Complement activation
- Mast cell degranulation
- Neutrophil chemotaxis
- Inflammation caused by immune cells
Type IV (delayed type hypersensitivity DTH) is caused by?
Activation of Th1 cells