Asthma pathophysiology

Cellular pathophysiology of asthma. Top, Cross-section of the normal airway and the asthmatic ain/vay. Mediators released during the inflammatory process associated with asthma cause bronchoconstriction, mucus secretion, and mucosal inflammation and edema. These changes reduce the size of the airway lumen and increase resistance to airflow, which leads to wheezing and shortness of breath. Bottom, The multitude of inflammatory cells (macrophages, eosinophils, mast cells, neutrophils) and neurotransmitters implicated in asthma pathophysiology. 

Fireman R 2003. Understanding asthma pathophysiology. Allergy Asthma Proc. 24 79-83. 

The p2-adrenergic receptor gene mutations have, therefore, been associated with a wide spectrum of respiratory phenotypes that include altered drug responses and bronchial hyperreactivity disease. The [l2-adrcncrgic receptor polymorphisms probably represent only a few of the genetic variables involved in asthma pathophysiology [157,165]. There may be potential to use these variants more widely to personalize diagnosis and treatment options. 

FIGURE 11-1. Steps for using your inhaler. (From Kelly HW, Sorkness CA. Asthma. In DiPiro JT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. New York McGraw-Hill 2005 515, with permission.)... 

From Kelly HW, Sorkness CA. Asthma. In DiPiro JT, Talbert RF, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 

O Inflammation plays a key role in the pathophysiology of COPD, but it differs from that seen in asthma therefore, the use of and response to anti-inflammatory medications are different. 

Palmer LJ, Cookson WOCM. Using single nucleotide polymorphisms (SNPs) as a means to understanding the pathophysiology of asthma. Respir Res 2001 2 102-112. 

The underlying pathophysiology of asthma is best described by which of the following statements ... 

Since elucidation of the sequences of the genes encoding the alr a2, and subtypes of adrenoceptors, it has become clear that there are relatively common genetic polymorphisms for many of these receptor subtypes in humans. Some of these may lead to changes in critical amino acid sequences that have pharmacologic importance. Often, distinct polymorphisms occur in specific combination termed haplotypes. Some of these polymorphisms have been consistently shown to alter the susceptibility to diseases such as heart failure, to alter the propensity of a receptor to desensitize, and to alter therapeutic responses to drugs in diseases such as asthma. This remains an area of active research because studies have reported inconsistent results as to the pathophysiologic importance of some polymorphisms. 

Barrios R et al Asthma Pathology and pathophysiology. Arch Pathol Lab Med 2006 130 447. [PMID 16594736]... 

Nearly all cells express kinin receptors that mediate the activities of both bradykinin and kallidin. The activation of these G-protein coupled receptors causes relaxation of venular smooth muscle and hypotension, increased vascular permeability, contraction of smooth muscle of the gut and airway leading to increased airway resistance, stimulation of sensory neurons, alteration of ion secretion of epithelial cells, production of nitric oxide, release of cytokines from leukocytes, and the production of eicosanoids from various cell types [11,12]. Because of this broad spectrum of activity, kinins have been implicated as an important mediator in many pathophysiologies including pain, sepsis, asthma, rheumatoid arthritis, pancreatitis, and a wide variety of other inflammatory diseases. Moreover, a recent report demonstrated that bradykinin B2 receptors on the surface of human fibroblasts were upregulated three-fold beyond normal in patients with Alzheimer s disease, implicating bradykinin as a participant in the peripheral inflammatory processes associated with that disease [13]. 

Eosinophils are known to play a role in the pathophysiology of allergic diseases, especially asthma (Frigas and Gleich 1986 Barnes 1989). They infiltrate the... 

Frigas E, Gleich GJ (1986) The eosinophil and the pathophysiology of asthma. J Allergy Clin Immunol 77(4) 527-537... 

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