Asthma Flashcards
Pathophysiologic abnormality of asthma
Airway hyperresponsiveness
Major risk factor for asthma
Atopy
Seen in 80% of asthmatic patients
Allergic rhinitis
Sensitizing allergens
Proteins with protease activity
Independent risk factor for women with asthma
Obesity
Late-onset asthma with concomitant nasal polyps
Intrinsic asthma
Activated by inhaled allergens that release inflammatory mediators
IgE in mast cells
MCC of perennial allergens
Dermatophagoides
Animal dander proteins
Cockroaches
MCC of seasonal allergens
Grass pollen
Ragweed
Tree pollen
Fungal spores
MC trigger of acute severe exacerbations
Viral URTI
Common trigger of asthma particularly in children
Exercise
Mechanism of EIA
Hyperventilation leading to increased osmolality of airway fluids
ABG: respi acid
Prevention of EIA
B2 agonists and antileukotrienes prior to exercise
Best prevention: regular treatment with ICS
Recommended for patients with aspirin-induced asthma
Salicylate-free diet
2 types of asthma
Allergic asthma
Idiosyncratic/Intrinsic
Allergic Asthma
(+) personal and/or family hx of allergic diseases
(+) wheal and flare skin reactions to ID injections
Inc level of serum IgE
(+) Response to provocation test
Intrinsic Asthma
Adult-onset, non atopic, MORE SEVERE and persistent
(-) Personal and/or Fam Hx of allergy
(-) skin tests
(+) Nasal polyps
(+) Aspirin-sensitivity
N serum IgE but may have Inc IgE in airways due to staph enterotoxins
Characteristic histo finding
Thickening of the BM due to subepithelial collagen deposition
Pathology of asthma
Uniform regardless of type, changes do not extend to the lung parenchyma
Characteristic of asthmatic airways
Eosinophil infiltration
Phenotype predominant in asthmatics
TH2 (releases IL5 inc IgE formation)
Major target cells of ICS
Epithelial cells
Pro inflammatory cytokines associated with more severe disease
TNF a, IL 1B
Mechanisms of AHR from epithelial damage
Loss of barrier function allowing penetration of allergens
Loss of enzymes degrading inflammatory mediators
Loss of relaxant factor
Exposure of sensory nerves
Structural changes in the airways that may lead to irreversible narrowing
Inc airway smooth muscle
Fibrosis
Angiogenesis
Mucus Hyperplasia
Confirms airflow limitation in asthma
Spirometry
Decreased FEV1, FEV1/FVC, PEF
Reversibility of spirometry in asthma
> 12% and 200mL INCREASE in FEV1 15 mins after and inhaled short-acting B2-agonist
(in some, 2-4 week trial of pred or prednisolone 30-40mg daily)
Test for airway responsiveness
AHR: induced by methacholine or histamine challenge calculating the provocative concentration that reduces FEV1 by 20% (PC20)
Three classes of bronchodilators
B2-adrenergic agonists
Anticholinergics
Theophylline
MOA of bronchodilators
Reverse bronchoconstriction, relaxation of airway smooth muscle
Most effective bronchodilators
B2 agonists
Duration of action of SABAs
Albuterol, Terbutaline
3-6 hours
As PRN meds
Duration of LABAs
Salmeterol, Formoterol
Over 12 hours, given BID
*never given in the absence of ICS
MC AE of B2 agonists
Muscle tremor and palpitations
Prevent cholinergic nerve-induced bronchoconstriction and mucus secretion
Anti-cholinergics (ipratropium, tiptropium)
*used only as add-on bronchodilators not controlled by LABA + ICS
MC reason for refractory asthma
Noncompliance
