NR507 week 1 edapt guide
Advanced Pathophysiology
(Chamberlain University)
, Week 1:Edapt Notes
1.
-Immediate hypersensitivity is mediated by IgE antibodies, which resulting an allergy, anaphylaxis, or
atopic disease. The NP should expect the client to have a type 1 hypersensitivity to recent medication
use, which can include these immediate reactions as clinical manifestations: urticaria, wheezing,
vomiting, and diaphoresis.
2. are the primary effector cells and are responsible for initiating and mediating
hypersensitivity reactions.
- Mast cells, type 1
characterized by the rapid release of proinflammatory mediators like histamines, leukotrienes,
and cytokines in response to allergen exposure, mast cells are the primary effector cells
responsible for initiating and mediating type 1 hypersensitivity reactions.
3. hypersensitivity reactions involve the formation of that can deposit in tissues,
leading to complement activation, inflammation, and tissue destruction.
-Type 3, immune complexes
- Type 3 hypersensitivity reactions involve the formation of immune complexes that can deposit in
tissues, leading to complement activation and inflammation. This process can cause tissue damage and
is associated with systemic lupus erythematosus (SLE) and serum sickness. Type 1 reactions are
mediated by IgE antibodies, and type 2 are mediated by IgG or IgM antibodies. Type 4 reactions are
activated by T- helper cells.
Type 1 = Mediated by IgE antibodies
,Anaphylactic Reaction
1. Antigen
2. B-cell
3. Plasma cell
4. IgE
5. Mast cell
6. Histamine
A type 1 reaction is mediated by IgE antibodies.
Type 2 = mediated by IgG or IgM antibodies
1. Anti-A antibodies in type B blood mix with type A blood
2. Antibodies attach to surface antigen of type A RBC
3. Complement activated; type A RBC cell wall attacked
4. Lysis of type A RBC
5. Phagocytosis
A type 2 cytotoxic reaction is mediated by IgG or IgM antibodies.
Type 3 = mediated by immune complexes
, 1. Antibodies bind to antigens
2. Immune complexes form
3. Complexes deposit in blood vessels or tissues
4. Activation of complement
5. Inflammatory response at the site of deposit
6. Release of lysosomal enzymes and chemical mediators
7. Tissue damage
A type 3 reaction is mediated by immune complexes.
Type 4 = mediated by cellular response.
1. Macrophage presents antigen
2. Sensitization of T lymphocyte
3. Release of lymphokines
4. Inflammation and lysis of antigen-bearing cells in the tissue
5. Tissue destruction
A type 4 delayed reaction is mediated by cellular response.
Advanced Pathophysiology
(Chamberlain University)
, Week 1:Edapt Notes
1.
-Immediate hypersensitivity is mediated by IgE antibodies, which resulting an allergy, anaphylaxis, or
atopic disease. The NP should expect the client to have a type 1 hypersensitivity to recent medication
use, which can include these immediate reactions as clinical manifestations: urticaria, wheezing,
vomiting, and diaphoresis.
2. are the primary effector cells and are responsible for initiating and mediating
hypersensitivity reactions.
- Mast cells, type 1
characterized by the rapid release of proinflammatory mediators like histamines, leukotrienes,
and cytokines in response to allergen exposure, mast cells are the primary effector cells
responsible for initiating and mediating type 1 hypersensitivity reactions.
3. hypersensitivity reactions involve the formation of that can deposit in tissues,
leading to complement activation, inflammation, and tissue destruction.
-Type 3, immune complexes
- Type 3 hypersensitivity reactions involve the formation of immune complexes that can deposit in
tissues, leading to complement activation and inflammation. This process can cause tissue damage and
is associated with systemic lupus erythematosus (SLE) and serum sickness. Type 1 reactions are
mediated by IgE antibodies, and type 2 are mediated by IgG or IgM antibodies. Type 4 reactions are
activated by T- helper cells.
Type 1 = Mediated by IgE antibodies
,Anaphylactic Reaction
1. Antigen
2. B-cell
3. Plasma cell
4. IgE
5. Mast cell
6. Histamine
A type 1 reaction is mediated by IgE antibodies.
Type 2 = mediated by IgG or IgM antibodies
1. Anti-A antibodies in type B blood mix with type A blood
2. Antibodies attach to surface antigen of type A RBC
3. Complement activated; type A RBC cell wall attacked
4. Lysis of type A RBC
5. Phagocytosis
A type 2 cytotoxic reaction is mediated by IgG or IgM antibodies.
Type 3 = mediated by immune complexes
, 1. Antibodies bind to antigens
2. Immune complexes form
3. Complexes deposit in blood vessels or tissues
4. Activation of complement
5. Inflammatory response at the site of deposit
6. Release of lysosomal enzymes and chemical mediators
7. Tissue damage
A type 3 reaction is mediated by immune complexes.
Type 4 = mediated by cellular response.
1. Macrophage presents antigen
2. Sensitization of T lymphocyte
3. Release of lymphokines
4. Inflammation and lysis of antigen-bearing cells in the tissue
5. Tissue destruction
A type 4 delayed reaction is mediated by cellular response.
