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15 Cards in this Set
- Front
- Back
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what is the Pathobiology of Asthma
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-increased vascular perm and edema
-mucus secreation -bronchoconstriction bronchial hyperreactivity |
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what are the risk factors for astham
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lack of endotoxin exposure
flagellin and defensin mutation (atopy and adam 33) TH2 polarization: drive the response to the trigger |
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what type of cells are classically associated with Asthma?
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eosinophils
(Dr. anderson also likes macrophages--release freee radicals--> inflamation-->damage (activated during astham symp |
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how do mast cells become activated and release inflammatory mediators?
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by the binding of Ag specific IgE to membrane
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What is the role of TH1 cells?
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to activate macrophages, CTLs, etc; arent doing the killing, but ordering the hit
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what is the role of TH2 cells?
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to secrete IL-4, IL-5, IL-13 in response to activation when Ag binds its recptor. TH2 promotes class switching to IgE--> activates mast cells
recruits eosinophils, mucous prod, airway hyperresponse |
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What type of response does TH17 promote?
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neutrophilic response, by secretion of IL 17
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What is the classic IgE mediated disease?
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Anaphylaxis
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What causes the "second wave" of inflamation in anaphylaxis?
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cysteinyl leukotrienes
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how are leukotrienes generated?
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arachidonic acid is acted upon by 5-lipo-->leuko A4 which isconvertedn to leuko c4/B4, transported out of cell
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what happens when Leukos bind receptor?
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increase sm contraction, edema, migration of eosinophils or increaseed airway secretion
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what are 2 leuko antagonists and their MOA?
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Zileuton- 5 lipo blocker
montelukast- blocks receptor site |
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when ag specific IgE binds to receptor on mast cell, what is relased?
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histamine
TNFa proteases heparin minutes to hours later: leukos and prostaglandins |
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what are some specific triggers fr asthma?
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ragweed
dust mees cats |
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what are some non specific triggers for asthma?
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smoke
cold air exercise |
