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