Hypersensativity Flashcards
Type 1 hypersensitivity
Immediate
1st exposure = Proliferation of IgE antibody which results in vasoactive amines and priming of mast cells
- TH2 mediated response
2nd exposure = recruitment of inflammatory cells and activation of mast cells
Histological lesions
- vascular dilation
- edema
- increased mucus production and inflammation
Known disorders
- anaphylaxis reactions
- bronchial asthma
- allergies
Type 2 hypersensitivity
Antibody mediated
Production of IgG/ IgM binds to antigen on target cell tissues and promotes phagocytosis and lysis of targeted cell
- activation of compliment by Fc receptors on IgG/IgM induces phagocytosis
Histologic lesions
- phagocytosis and lysis of cells
- inflammation and functional derangement without cell or tissue injuries
Known disorders associated = autoimmune anemia and good pasture syndrome, MG, TPP, rheumatic fever, pernicious anemia, pemphigus vulgaris
Type 3 hypersensitivity
Immune complex mediated
Deposition of antigen-antibody complexes which leads to compliment activation and recruitment of leukocytes by compliment products and Fc receptors
- releases enzymes and other toxic molecules into the blood stream
Histologic lesions
- inflammation
- necrotizing vasculitis and fibrinoid necrosis
Disorders associated
- SLE
- glomerulonephritis
- serum sickness
Type 4 hypersensitivity
Cell-mediated
Activated T lymphocytes release cytokines and procure inflammation and recruitment of macrophages and CD8 T cells
- later macrophages and CD8-Tcells initiate cytotoxicity
Two types of Tcell reactions:
- 1) cytokine mediated CD4-Tcell
- 2) direct cytotoxic CD-8 T cells
Histologic lesions
- perivascular infiltrates
- edema
- granuloma formation
- cell destruction
Conditions associated
- contact dermatitis
- MS
- DM type 1
- TB activation
3 events of immediate response in type 1
1) activation of TH2 cells Na production of IgE
2) sensitization of mast cells by IgE antibodies
3) activation of mast cells and release of mediators including vasoactive amines
Immediate vs late phase reactions
Immediate:
- occurs within 30 minutes after allergen exposure
- goes away within 60 minutes
- stimulated by mast cell granule contents and lipid mediators
Late-phase
- occurs 2-8 hrs later and lasts several days
- stimulated by cytokines
- shows inflammation and tissue damage
Dermatographic urticaria
is also called “skin writing”
Caused by release of histamine from mast cells without antigen exposure
Basic skin scratches result in over activation of hypersensitivity
Treatment = antihistamines if needed, otherwise benign
Solar urticaria
“Sun allergies”
Acute sun exposure results in over hypersensitivity of histamine release from mast cells and causes a sunburn appearance
Cholinergic urticaria
Type 1 hypersensitivity reaction to generalized heat
Veritable symptoms but can be life-threatening
Cold urticaria
“Cold allergy”
Unknown cause of hypersensitivity type 1 due to cold
Variable symptoms but can be life threatening
Insect bites and stings
Are usually an example of type 1 hypersensitivity to the toxin released from the bite
- NOT heavily histamine driven but more allergy to the toxin driven
Can occasionally be type 4 response if delayed symptoms
Allergic contact dermatitis
Is usually type 4 but can be type 1
- type 1 = almost instantaneously
- type 4 = takes a couple days
Principal mediates of hypersensitivity are what?
Histamine, proteases, PGE and leukotrienes
3 phases of type 3 hypersensitivity
1) formation of immune complexes
2) deposition of immune complexes
3) inflammation and tissue injury
