Hypersensitivity 1 and 2 Flashcards
Hypersensitivity:
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):
- Allergen specific IgE.
- Mast cells.
- Allergen.
- Eosinophils.
- 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):
- First exposure to allergen.
- Antigen activation of Th2 cells and stimulation of IgE class switching in B cells (IL-4).
- Production of IgE.
- 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:
Cytokines.
Biologic effects of histamines (2):
- Vasodilation.
2. Vascular leak.
Biologic effects of lipid mediators (2):
- Broncho-constriction.
2. Intestinal hypermotility.
Biologic effects of cytokines:
Inflammation.
Biologic effects of enzymes:
Tissue damage.
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):
- Allergic rhinitis.
- Allergic asthma.
- Eczema or atopic dermatitis.
- Some food allergy.
- Some drug allergy.
- Insect venom allergy.
Allergic march:
Progression of allergic symptoms with age.
Allergen-specific serum IgE test:
- Plate (solid phase) coated with allergen.
- Patient’s serum added.
- Labeled anti-IgE added.
Serum IgE levels - ELISA method:
- Solid surface coated with anti-IgE antibody.
- Patient’s serum added.
- 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:
ADCC
- IgG antibodies serve as “bridges” to link target cells to effector cells.
Mechanisms of Type II hypersensitivity (3):
- Complement and Fc receptor mediated inflammation (ADCC).
- Opsonization and phagocytosis.
- Abnormal physiologic responses without cell/tissue injury.
Disease associations of Type II hypersensitivity (6):
- Transfusion reaction.
- Hemolytic disease of the newborn.
- Autoimmune hemolytic anemia.
- Goodpasture syndrome.
- Pemphigus vulgaris.
- 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):
- Hemolytic disease of the newborn.
- Autoimmune hemolytic anemia.
- 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 banking:
- Cross-matching.
- Blood typing.
- Ab detection.
- Ab identification.
Clinical symptoms of a transfusion reaction (4):
- Fever.
- Low BP.
- Nausea and vomiting.
- Back and chest pain.
Hemolytic disease of the newborn:
Erythroblastosis fetalis:
- 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):
- Elevated bilirubin.
- Large liver and spleen.
- Petechiae.
- Positive direct Coombs test.
Autoimmune hemolytic anemia:
AIHA
- Pt’s produce anti-RBC antibodies.
- Can cause hemolysis of RBCs.
- Positive direct Coombs test.
Pemphigus vulgaris:
- Disease of skin and mucous membranes.
- Causes blisters all over body.
- Autoantibodies against intercellular cement substance of skin and mucous membranes.
Goodpasture’s syndrome:
- Targets basement membranes of kidney glomeruli and lung alveoli.
- Leads to acute glomerulonephritis and pulmonary hemorrhage.
Acute rheumatic fever:
- Follows a throat infection with group A strep.
- Symptoms present about 2-4 weeks following onset of infection.
- JONES
- Molecular mimicry with cardiac antigens.
