Ch. 11 Hypersensitivity Flashcards
1
Q
Type 1 - Immediate hypersensitivity
A
- aka allergy
- mediated by eosinophils and mast cells
- first exposure IgE cells are produced and bind to mast cells
- next exposure antigens crosslink IgE on mast cell and lead to degranulation
- leads to vascular dilation and smooth muscle construiction
- production of cytokines to recruit neutrophils and eosinophils
- TNF - neutrophil, IL-4 IgE
- IL-5 activates eosinophil
- inflammation causes tissue damage
2
Q
Th2 response in Immediate
A
- Interactions with some antigens stimulates Th2 response leading to creation of IgE and eosinophil activation (only certain individuals)
- IgE binds to the mast cells via Fc receptor
- leads to immediate hypersensitivity next time there is an exposure
3
Q
sensitization
A
- coating mast cells with IgE on first exposure
4
Q
3 results of Mast cell activation by cross linking of IgE
A
- Degranulation:
- Vasoactive amines (histamine) - vascular dilation, smooth muscle contraction
- proteases - tissue damage
- Lipid mediator synth. and secretion (arachidonic acid metabs)
- prostaglandins - vascular dilation
- leukotrines - smooth muscle contraction
- Cytokines - late phase attracts leukocytes
- TNF and IL-4 - neutrophil and eosinophil rich inflammation
- Th2 recruited, secretes more cytokines - IL-5 activates more eosinophils
5
Q
treatments of immediate hypersensitivity
A
- allergic sinusitis (hay fever) and food allergies
- desensitization, Anti-IgE antibody, antihistamines
- Bronchial Asthma - smooth muscle contraction of airways
- corticosteroids
- Anaphylaxis Shock - airway obstruction edema in larynx (widespread mast cell degranulation), fall in bp
- Epinephrine
6
Q
Type II Antibody mediated
A
- Antibodies (IgM or IgG) bind to tissues and target them for damage - autoantibodies
- usually target a specific tissue type
- promote phagocytosis of cells and activate complement and inflammation
7
Q
type III immune complex mediated
A
- They tend to deposit in high bp areas - kidney and turbulence - blood vessel split
- widespread vasculitis, arthritis, nephritis
- auto-antibodies
- vasculitis - inflammation and damage in blood vessels where the complement and antibodies depsosit
8
Q
Mechanism for II/III damage
A
- inflammation
- IgG - neutrophil and macrophage recruitment
- IgM - complement activation
- opsonization
- interfering with normal function
9
Q
Autoimmune hemolytic anemia
A
- Antibodies against RBC - opsonization and phagocytosis
10
Q
Autoimmune thrombocytopenic purpura
A
- autoantibodies against platelets - opsonization and phagocytosis
11
Q
pemphigus vulgaris
A
- autoantibodies against epidermal cadherin in junction
- skin bullae and vesicles
- disrupts intracellular adhesion
12
Q
Goodpasture’s syndrome
A
- antibodies against proteins in basement membrane of kidney glomerulus and lung aveoli
- nephritis and lung hemorrhages
13
Q
rheumatic fever
A
antibodies against strept bacteria cross reacts with an antigen in the heart
- myocarditis
14
Q
Myasthenia gravis
A
antibody against Ach receptor - inhibits Ach signalling
- muscle weakness and paralysis
15
Q
Grave’s disease
A
antibody against TSH receptor
- hyperthyroidism