Asthma and Allergic Reactions Study Notes

Frank's Asthma and Allergic Reactions: Study Notes

• Chest Tightness Basis: Inspiration creates negative airway pressure, enlarging airways. Expiration narrows them, exacerbated by inflammation and bronchoconstriction (as in asthma). Trapped air increases residual lung volume, requiring increased effort, leading to chest tightness. This high residual volume results in hyperinflation, visible on chest X-rays.

• Radiographic Findings: Hyperinflated chest, peribronchial markings (inflammation around the airways) are characteristic of asthma.

• Asthma Treatment Ineffectiveness: Asthma involves more than just smooth muscle constriction. Airway inflammation (cellular infiltration, mucus secretion, swelling) is a significant factor. Bronchodilators address only smooth muscle constriction; they are not effective in reversing chronic airway inflammation. Steroids target the inflammatory response.

• Eosinophilia Basis: Allergic individuals favor a TH2 immune response over TH1, resulting in increased IL-4 and IL-13 production (triggering IgE). IL-5, also from TH2 cells, promotes eosinophil maturation. CCL11 (eotaxin) attracts eosinophils to the airways. This interplay explains the link between IgE and eosinophilia.

• Wheal-and-Flare Reaction: Allergen skin tests induce a wheal-and-flare reaction in allergic individuals within 10-20 minutes. This reaction is due primarily to mast cell histamine release. Histamine increases blood vessel permeability (wheal), and blood vessel dilation creates redness (flare).

• Late Phase Response: Redness and swelling recurring at skin test sites 24 hours later indicate a cellular infiltrate, a late-phase reaction, following the initial allergic reaction.

• NSAIDs and Asthma: Nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin and ibuprofen can trigger wheezing in some patients. Inhaling an allergen or NSAID leads to a different pathway; this triggers an increase in leukotriene production.

• Immunotherapy Mechanism: Immunotherapy aims to shift the immune response from TH2 (allergy-associated) to TH1 (anti-allergy) by repeated allergen exposure. This reduces IgE by promoting an IgG response and inhibiting mast cell and B-cell activation.

• Allergic Reactions in Vaccinated Children: Despite repeated immunizations with protein antigens (e.g., tetanus toxoid), atopic children rarely develop allergic reactions. This is due to the difference in antigen presentation in vaccines compared to allergic exposures. Large-dose subcutaneous vaccination favors a TH1 response (and therefore IgG), while allergic exposures favor a TH2 response (and increased IgE) due to different antigen presentation methods (low dose, mucosal exposure).