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what causes intrinsic allergies?
non-allergenic activities (e.g. exercise) - IgE-independent
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what causes extrinsic allergies?
allergens that are inhaled - IgE-dependent
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what is the definitive test for asthma?
- methacholine challenge
- asthma triad of symptoms
- bronchoconstrictionmucus production
- fluid accumulation (edema)
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what 3 cytokines released by TH2 activate B cells?
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what are some features of airway remodeling?
- more goblet cells
- fewer cilia
- submucosal gland hypertrophy
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cilia beat slower at which airway: distal or proximal?
distal
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histamine: site of action and function
- site: airway smooth muscle
- function: bronchoconstriction
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prostaglandins: site of action and function
- site: glands
- function: mucus secretion
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leukotrienes: site of action and function
- site: capillaries
- function: edema
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what allergenic mediators are responsible for bronchoconstriction?
histamine, bradykinin, Leukotrienes
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which mediator produces bronchoconstriction via C-fiber stimulation?
bradykinin
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what is the function of C-fibers?
stimulated by allergenic mediators to cause reflex bronchoconstriction and local release of neuropeptides
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in asthma, the SNS causes: relaxation or bronchoconstriction? how?
- relaxation
- releases ACh/NE to activate beta-2 receptors
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what are the 2 mediators of NANC-I?
VIP and NO
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does NO cause bronchoconstriction or relaxation?
- both
- relaxation (dilation) at low levels and constriction at high levels
-
this parasympathetic mediator causes bronchodilation at low levels and bronchoconstriction at high levels
NO
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which is associated with O2 radicals and inflammation: eNOS or iNOS?
iNOS
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which is present in nanomolar concentrations: eNOS or iNOS?
iNOS
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which mast cell mediator degrades VIP leading to increased ACh effects and bronchoconstriction?
tryptase
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what are the 2 mediators of NANC-E?
substance P and neurokinin A (tachykinins)
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what are the steps of the early phase of asthma?
- 1. antigen inhalation --> phagocytosis by macrophages
- 2. macrophages present antigen to T cells --> activation of B cells
- 3. B cells release IgE
- 4. antigen cross-links with mast cells to activate C-fibers
- 5. mast cell degranulation --> symptom triad (constriction, mucus, edema) and chemotaxis
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what are the steps of the late phase of asthma?
- 1. leukocyte degranulation
- 2. bronchoconstriction and inflammation
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MOA of glucocorticoids
decrease late phase rxn by activating adenyl cyclase --> relaxation and reduced mast cell mediator release
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which drug class works by activating adenyl cyclase?
glucocorticoids
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do glucocorticoids affect the early or late phase of asthma response?
late
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oral thrush and dysphonia are associated with which asthma drug(s)?
glucocorticoids
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IgG monoclonal antibody that decreases sensitivity to inhaled allergens
omalizumab
-
omalizumab MOA
depletes free IgE on basophils, mast cells and dendritic cells
-
omalizumab indication
>11 yrs when glucocorticoids are not effective
-
omalizumab s/e
- anaphylaxis (rare)
- decreased cancer responsiveness
-
ADCC preferentially uses: IgE, IgG or IgM?
IgE
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MOA of ADCC
IgE binds to NK cell to direct it to the targeted cell to be killed
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MOA of specific allergen immunotherapy (SIT)
- -induces CD4CD25 (regulatory) T cells so tolerance occurs
- -cellular immune response instead of humoral
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specific allergen immunotherapy (SIT) induces which type of immune cells?
CD4CD25 (regulatory) T cells
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sublingual allergen immunotherapy is more effective for seasonal or perennial allergies?
seasonal
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indication for Oralair?
allergic rhinitis in response to any of 5 grass pollens
-
what causes food allergy?
immune response to food proteins
-
nonspecific vs specific mechanism of food allergy
- nonspecific: mucin coat in GI tract prevents absorption of antigens
- specific: IgA neutralizes antigens
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which Ig is associated with food allergies: IgE, IgG or IgA?
IgA
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major immune cell involved with food allergies
basophils
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tx for food allergies?
PO and SL immunotherapy (SIT)
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