Pathophysiology of chronic and acute asthma exacerbations

Nursing - Asthma

The limitation of airflow in asthma is reported as "recurrent and caused by a variety of changes in the airway." (Expert Panel Report 3, National Heart, Lung, and Blood Institute, 2007, p.1) Those changes include: (1) bronchoconstriction; (2) airway edema; (3) airway hyperresponsiveness; and (4) airway remodeling. Expert Panel Report 3, National Heart, Lung, and Blood Institute, 2007, p.1) Airway edema occurs with the progression of the disease and the inflammation is more progressive and exacerbated by "edema, inflammation, mucus hypersecretion and the formation of inspissated mucus plugs as well as structural changes including hypertrophy and hyperplasia of the airway smooth muscle." (Expert Panel Report 3, National Heart, Lung, and Blood Institute, 2007, p.1) Airway hyperresponsivenss is reported to be "an exaggerated bronchoconstrictor response to a wide variety of stimuli. Airway modeling speaks of the permanent structural changes in the airway reported to be associated with "loss of lung function that is not prevented by or fully reversible by the current therapy." (Expert Panel Report 3, National Heart, Lung, and Blood Institute, 2007, p.1)

Pathophysiology of Chronic Asthma

Factors that limit airway flow in acute and persistent asthma include environmental factors and inflammatory products. Airway narrowing and the following interference with airflow are the clinical symptoms in the physiological event. Allergen-inducted acute bronchorestriction is stated to result from "IgE-dependent release of mediators from mast cells that includes histamine, tryptase, leukotrienes, and prostaglandins that directly contract airway smooth muscle." (Expert Panel Report 3, National Heart, Lung, and Blood Institute, 2007, p.1)

Genetics Impact on Pathophysiology of Chronic Asthma and Acute Asthma Exacerbation

It is reported that susceptibility genes are believed to be inclusive of those for T-helper cells types 1 and 2, IgE interleukins (IL-3, -4, -5, -9, -13), granulocyte-monocyte colony-stimulating factor (GM-CSF), tumor necrosis factor-? (TNF-?), and the ADAM33 gene, which may stimulate airway smooth muscle and fibroblast proliferation or regulate cytokine production." (Merck Manual, 2013, p.1) It is reported that genetic and environmental components "may interact by "determining the balance between T. h 1 and T. h2 cell lineages. Infants may be born with a predisposition toward proallergic and proinflammatory T. h 2 immune responses, characterized by growth and activation of eosinophils and IgE production. Early childhood exposure to bacterial and viral infections and endotoxins may shift the body to T. h 1 responses, which suppresses T. h 2 cells and induces tolerance." (Merck Manual, 2013, p.1) Morrow (2007) reports that there are no "limited examples of gene polymorphisms that can influence responses to beta-2 agonists, glucocorticosteriods and leukotriene modifiers in patients with asthma." (p.457) Morrow additionally states that gene mutations that alter the response to asthma therapy are inclusive of: (1) Arg/Arg atr position 16; (2) mutations of LTC4S; (3) ALOX5; (5) GR/NR3C1; (6) increased expression of GR; (7) CRHR1 variants; (8) mutations in CYP1A2; and (9) T314 allele for histamine N-mathyltransferase. (Morrow, 2007, p. 457) Reported as some of the effects that are linked to these mutations are a response to therapy that is either decreased or increased, resistance of glucocorticoid, theophylline clearance decrease and potential toxicity as well as increases in bronchoconstriction. (Morrow, 2007, paraphrased)