Flashcards in Hypersensitivity 1 and 2 Deck (31):
An exaggerated response resulting i harm to the host.
Type I hypersensitivity results in:
Release of mediators from IgE-sensitized mast cells.
Components of Type I hypersensitivity immediate reaction (5):
1. Allergen specific IgE.
2. Mast cells.
5. CD4+ Th2 cells
Type I hypersensitivity late-phase:
Develops more slowly, characterized by the accumulation of neutrophils, eosinophils and macrophages.
Type I hypersensitivity - sensitization (4):
1. First exposure to allergen.
2. Antigen activation of Th2 cells and stimulation of IgE class switching in B cells (IL-4).
3. Production of IgE.
4. Binding of IgE to FC receptors on mast cells.
Mediators of the Type I hypersensitivity immediate reaction:
- Vasoactive amines (histamine).
- Lipid mediators.
Mediators of the Type I hypersensitivity late-phase reaction:
Biologic effects of histamines (2):
2. Vascular leak.
Biologic effects of lipid mediators (2):
2. Intestinal hypermotility.
Biologic effects of cytokines:
Biologic effects of enzymes:
Type I hypersensitivity late phase reaction(3):
- IL-5 from mast cells and Th2 cells recruit and activate eosinophils.
- Eosinophils release additional mediators.
- Begins within 4-8 hours and lasts 1-2 days.
Disease states caused or affected by Type I hypersensitivity (6):
1. Allergic rhinitis.
2. Allergic asthma.
3. Eczema or atopic dermatitis.
4. Some food allergy.
5. Some drug allergy.
6. Insect venom allergy.
Progression of allergic symptoms with age.
Allergen-specific serum IgE test:
1. Plate (solid phase) coated with allergen.
2. Patient's serum added.
3. Labeled anti-IgE added.
Serum IgE levels - ELISA method:
1. Solid surface coated with anti-IgE antibody.
2. Patient's serum added.
3. Labelled anti-IgE added.
Type II hypersensitivity:
- Antibody mediated hypersensitivity.
- Involves IgM or IgG antibodies.
- Involves a circulating antibody and its target antigen.
- Antigen is located either on the surface of a cell in circulation or in a tissue.
Antibody-dependent cell-mediated cytotoxicity:
- IgG antibodies serve as "bridges" to link target cells to effector cells.
Mechanisms of Type II hypersensitivity (3):
1. Complement and Fc receptor mediated inflammation (ADCC).
2. Opsonization and phagocytosis.
3. Abnormal physiologic responses without cell/tissue injury.
Disease associations of Type II hypersensitivity (6):
1. Transfusion reaction.
2. Hemolytic disease of the newborn.
3. Autoimmune hemolytic anemia.
4. Goodpasture syndrome.
5. Pemphigus vulgaris.
6. Rheumatic fever.
Direct Coombs test:
Picks up antibodies directly on the surface of the red blood cell:
- Pt's blood added to anti-Ig leads to agglutination of RBC.
Direct Coombs test is used to diagnose (3):
1. Hemolytic disease of the newborn.
2. Autoimmune hemolytic anemia.
3. Transfusion reaction.
Indirect Coombs test:
Measures anti-RBC antibodies in the serum.
- Uncoated RBCs added to serum from pt with antibodies, anti-Ig added, agglutination of RBC.
Main use of indirect Coombs test:
- Blood typing.
- Ab detection.
- Ab identification.
Clinical symptoms of a transfusion reaction (4):
2. Low BP.
3. Nausea and vomiting.
4. Back and chest pain.
Hemolytic disease of the newborn:
- Dramatic type II reaction.
- Antigen present on the surface of the red cell, RhD.
- Occurs in second pregnancy of woman who is RhD- and has RhD+ baby.
Hemolytic disease of the newborn if untreated causes (4):
1. Elevated bilirubin.
2. Large liver and spleen.
4. Positive direct Coombs test.
Autoimmune hemolytic anemia:
- Pt's produce anti-RBC antibodies.
- Can cause hemolysis of RBCs.
- Positive direct Coombs test.
- Disease of skin and mucous membranes.
- Causes blisters all over body.
- Autoantibodies against intercellular cement substance of skin and mucous membranes.
- Targets basement membranes of kidney glomeruli and lung alveoli.
- Leads to acute glomerulonephritis and pulmonary hemorrhage.