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Pathogenesis of Asthma: Theories of Asthma Pathogenesis

The pathogenesis of allergenic asthma has been described in two pathogenetic theories (Fig 1). The direct theory is derived from the original observations of allergists that some patients with allergic rhinitis, especially children, have atopic bronchospasm as well. Specific IgE-antibody is fixed to airways, and bivalent linking with specific antigen-E (pollen, dander) results in initiation of the synthesis and secretion of mediators of inflammation by respiratory mast cells. Histamine and other mediators cause bronchoconstriction by

Pathogenesis of Asthma: Introduction

Come degree of bronchomotor tone resulting from tonic cholinergic parasympathetic activity is present in all normal individuals. Asthma is distinguished from the normal bronchoconstrictor response by the suddenness and severity with which bronchomotor tone increases. Life-threatening bron-choconstriction can occur in minutes; asthmatic bronchospasm may also remit spontaneously, sometimes for many years between “attacks.”

Airway Remodeling in Severe Asthma

Studies of the airways of patients who die from asthma demonstrate thickened airway walls due to increases in smooth muscle mass, infiltration with inflammatory cells, deposition of connective tissue, vascular changes, and mucous gland hyperplasia, a condition that is termed airway remodeling. Airway remodeling may be a feature of milder and even asymptomatic asthma. The remodeling of airways can result in the worsening of airway narrowing, airflow obstruction, and disease progression. Airway remodeling in asthma

Targeting Improvements in Asthma Morbidity in Chicago: Quality Improvement

Supported by funding from The Otho S.A. Sprague Memorial Institute, a series of Chicago-area collaboratives were formed to assess current asthma care patterns and to use social networking theory to improve quality and reduce unwanted variation in care of asthma in Chicago. Three collaboratives were conducted: (1) the Chicago Emergency Department Asthma Collaborative (CEDAC), a 1-year collaborative with 21 participating EDs; (2) the Chicago-Area Hospital Asthma Collaborative, a 6-month collaborative with 17 participating hospitals; and

Targeting Improvements in Asthma Morbidity in Chicago: Consortia

CAC The CAC was formed in January 1996 as a collaborative effort of the ALAMC and the American College of Chest Physicians. The vision for the CAC was to bring individuals and organizations together as a community health network in an effort to work collectively, interdependently, and in synergy to combat the Chicago asthma epidemic. Cofounders Sydney Parker, PhD, and the late Alan Shaw, ALAMC Deputy Executive Director, envisioned an integrated network of regional leaders

Stydying of Occupational Asthma and Work-Exacerbated Asthma

The Research Ethics Board, the University Health Network, and the University of Toronto provided study approval. Patients with suspected WRA from a occupational lung disease clinic of a teaching hospital, with clinical visits from 2002 to 2004, and additional Ontario WSIB claimants from the same time period completed a questionnaire, which was slightly modified from that used in our pilot study. The questionnaire included age, education level, self-perception of work conditions, and physician factors related to diagnosis. It

Occupational Asthma and Work – Exacerbated Asthma

Approximately 13% of the Canadian adult population has been reported to have asthma, and, based on the answers to a questionnaire, 36% of those with adult-onset asthma had possible or probable “occupational asthma”. Asthma caused by exposure to an agent specific to a workplace and not to stimuli outside the work environment, is termed occupational asthma (OA), more strictly distinguishing it from coincidental/concurrent asthma that is aggravated or exacerbated at work, referred to as work-exacerbated