The current assignment focuses upon understanding the deep seated pathophysiology associated acute respiratory distress or failure. In this respect, developing a knowledge regarding the pathophysiology can help in the development of effective preventive measures as well as design a sound care plan. The pathophysiology here mainly focuses upon the aetiology and the causes of a disease. Therefore, understanding the pathophysiology helps in understanding the origin as well as identifies the genetic roots for the development of a disease within the patient population (Villar et al. 2014). Pathophysiology And Exacerbation Of Asthma Essay. It has been observed that most of the times the environment along with the genetic factors contributes towards the development of a disease (Khemani et al. 2015).  Therefore, a detailed knowledge of the pathophysiology helps to take into consideration all these factors and the different levels of expression produced by them.  In the current study, a particular case study has been taken into consideration. Based upon the conditions and the symptoms presented by the patient, the underlying pathophsyiology has been accessed.

Brief Summary Of The Patient’s Current Health Problem

Here, the patient is a 66 year old man Harry suffering from acute respiratory distress owing to which he had been admitted to the hospital. The respiratory distress emerged due to exacerbation of asthmatic conditions within the patient. As mentioned by Pediatric Acute Lung Injury Consensus Conference Group (2015), the falling of the SpO2 below 90% for longer periods of time could lead to medical emergency as the patient is unable to respire normally. In case the patient is left untreated for longer periods of time it could lead to respiratory failure and eventually death (Mac Sweeney and McAuley 2016). As mentioned by Lemiale  et al. (2015), with failure of the respiratory system, the neurological system will fail and the mental status of the patient deteriorates.

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Here,   the patient Harry was diagnosed with PaO₂ less than 60 mm of Hg without elevated CO₂level. In this respect, urgent resuscitation had to be provided to the patient, which involves airway control, ventilator management and stabilization of the circulation.Pathophysiology And Exacerbation Of Asthma Essay/  In this respect, a therapeutic plan needs to be developed for the patient based on informed clinical and laboratory examination (Pediatric Acute Lung Injury Consensus Conference Group 2015). The laboratory examination confirmed exacerbation of asthma within the patient.  The tests which were conducted upon the patients were a chest x- ray followed by a sputum tests. The chest x-ray depicted shrunken alveoli

Asthma is a common chronic disorder of the airways that involves a complex interaction of airflow obstruction, bronchial hyperresponsiveness and an underlying inflammation. This interaction can be highly variable among patients and within patients over time. This section presents a definition of asthma, a description of the processes on which that definition is based—the pathophysiology and pathogenesis of asthma, and the natural history of asthma. Pathophysiology And Exacerbation Of Asthma Essay.

Definition of Asthma

Asthma is a common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness, and an underlying inflammation (box 2-1). The interaction of these features of asthma determines the clinical manifestations and severity of asthma (figure 2-1) and the response to treatment.

Box 2-1

CHARACTERISTICS OF CLINICAL ASTHMA. ▪ Symptoms ▪ Airway obstruction ▪ Inflammation ▪ Hyperresponsiveness ▪ Symptoms

Figure 2-1

THE INTERPLAY AND INTERACTION BETWEEN AIRWAY INFLAMMATION AND THE CLINICAL SYMPTOMS AND PATHOPHYSIOLOGY OF ASTHMA

The concepts underlying asthma pathogenesis have evolved dramatically in the past 25 years and are still undergoing evaluation as various phenotypes of this disease are defined and greater insight links clinical features of asthma with genetic patterns (Busse and Lemanske 2001; EPR—2 1997). Central to the various phenotypic patterns of asthma is the presence of underlying airway inflammation, which is variable and has distinct but overlapping patterns that reflect different aspects of the disease, such as intermittent versus persistent or acute versus chronic manifestations.Pathophysiology And Exacerbation Of Asthma Essay.  Acute symptoms of asthma usually arise from bronchospasm and require and respond to bronchodilator therapy. Acute and chronic inflammation can affect not only the airway caliber and airflow but also underlying bronchial hyperresponsiveness, which enhances susceptibility to bronchospasm (Cohn et al. 2004).

Treatment with anti-inflammatory drugs can, to a large extent, reverse some of these processes; however, the successful response to therapy often requires weeks to achieve and, in some situations, may be incomplete (Bateman et al. 2004; O’Byrne and Parameswaran 2006). For some patients, the development of chronic inflammation may be associated with permanent alterations in the airway structure—referred to as airway remodeling—that are not prevented by or fully responsive to currently available treatments (Holgate and Polosa 2006). Therefore, the paradigm of asthma has been expanded over the last 10 years from bronchospasm and airway inflammation to include airway remodeling in some persons (Busse and Lemanske 2001).

The concept that asthma may be a continuum of these processes that can lead to moderate and severe persistent disease is of critical importance to understanding the pathogenesis, pathophysiology, and natural history of this disease (Martinez 2006). Although research since the first NAEPP guidelines in 1991 (EPR 1991) has confirmed the important role of inflammation in asthma, the specific processes related to the transmission of airway inflammation to specific pathophysiologic consequences of airway dysfunction and the clinical manifestations of asthma have yet to be fully defined. Similarly, much has been learned about the host–environment factors that determine airways’ susceptibility to these processes, but the relative contributions of either and the precise interactions between them that leads to the initiation or persistence of disease have yet to be fully established.Pathophysiology And Exacerbation Of Asthma Essay.  Nonetheless, current science regarding the mechanisms of asthma and findings from clinical trials have led to therapeutic approaches that allow most people who have asthma to participate fully in activities they choose. As we learn more about the pathophysiology, phenotypes, and genetics of asthma, treatments will become available to ensure adequate asthma control for all persons and, ideally, to reverse and even prevent the asthma processes.

As a guide to describing asthma and identifying treatment directions, a working definition of asthma put forth in the previous Guidelines remains valid: Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role: in particular, mast cells, eosinophils, T lymphocytes, macrophages, neutrophils, and epithelial cells. In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment. The inflammation also causes an associated increase in the existing bronchial hyperresponsiveness to a variety of stimuli. Reversibility of airflow limitation may be incomplete in some patients with asthma (EPR 1991; EPR—2 1997).

This working definition and its recognition of key features of asthma have been derived from studying how airway changes in asthma relate to the various factors associated with the development of airway inflammation (e.g., allergens, respiratory viruses, and some occupational exposures) and recognition of genetic regulation of these processes. From these descriptive approaches has evolved a more comprehensive understanding of asthma pathogenesis, the processes involved in the development of persistent airway inflammation, and the significant implications that these immunological events have for the development, diagnosis, treatment, and possible prevention of asthma. Pathophysiology And Exacerbation Of Asthma Essay.

Pathophysiology and Pathogenesis of Asthma

Airflow limitation in asthma is recurrent and caused by a variety of changes in the airway. These include:

• ▪ Bronchoconstriction. In asthma, the dominant physiological event leading to clinical symptoms is airway narrowing and a subsequent interference with airflow. In acute exacerbations of asthma, bronchial smooth muscle contraction (bronchoconstriction) occurs quickly to narrow the airways in response to exposure to a variety of stimuli including allergens or irritants. Allergen-induced acute bronchoconstriction results from an IgE-dependent release of mediators from mast cells that includes histamine, tryptase, leukotrienes, and prostaglandins that directly contract airway smooth muscle (Busse and Lemanske 2001). Aspirin and other nonsteroidal anti-inflammatory drugs (see section 3, component 3) can also cause acute airflow obstruction in some patients, and evidence indicates that this non-IgE-dependent response also involves mediator release from airway cells (Stevenson and Szczeklik 2006). In addition, other stimuli (including exercise, cold air, and irritants) can cause acute airflow obstruction. The mechanisms regulating the airway response to these factors are less well defined, but the intensity of the response appears related to underlying airway inflammation. Stress may also play a role in precipitating asthma exacerbations. The mechanisms involved have yet to be established and may include enhanced generation of pro-inflammatory cytokines. Pathophysiology And Exacerbation Of Asthma Essay.
• ▪ Airway edema. As the disease becomes more persistent and inflammation more progressive, other factors further limit airflow (figure 2-2). These include 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. These latter changes may not respond to usual treatment.
• ▪ Airway hyperresponsiveness. Airway hyperresponsiveness—an exaggerated bronchoconstrictor response to a wide variety of stimuli—is a major, but not necessarily unique, feature of asthma. The degree to which airway hyperresponsiveness can be defined by contractile responses to challenges with methacholine correlates with the clinical severity of asthma. The mechanisms influencing airway hyperresponsiveness are multiple and include inflammation, dysfunctional neuroregulation, and structural changes; inflammation appears to be a major factor in determining the degree of airway hyperresponsiveness. Treatment directed toward reducing inflammation can reduce airway hyperresponsiveness and improve asthma control.
• ▪ Airway remodeling. In some persons who have asthma, airflow limitation may be only partially reversible. Permanent structural changes can occur in the airway (figure 2-2); these are associated with a progressive loss of lung function that is not prevented by or fully reversible by current therapy. Airway remodeling involves an activation of many of the structural cells, with consequent permanent changes in the airway that increase airflow obstruction and airway responsiveness and render the patient less responsive to therapy (Holgate and Polosa 2006).Pathophysiology And Exacerbation Of Asthma Essay.  These structural changes can include thickening of the sub-basement membrane, subepithelial fibrosis, airway smooth muscle hypertrophy and hyperplasia, blood vessel proliferation and dilation, and mucous gland hyperplasia and hypersecretion (box 2-2). Regulation of the repair and remodeling process is not well established, but both the process of repair and its regulation are likely to be key events in explaining the persistent nature of the disease and limitations to a therapeutic response.

Figure 2-2

FACTORS LIMITING AIRFLOW IN ACUTE AND PERSISTENT ASTHMA Source: Adapted and reprinted from The Lancet, 368, Holgate ST, Polosa R. The mechanisms, diagnosis, and management of severe asthma in adults, 780–93. Copyright (2006), with permission from (more…)

Box 2-2

FEATURES OF AIRWAY REMODELING. ▪ Inflammation ▪ Mucus hypersecretion ▪ Subepithelial fibrosis ▪ Airway smooth muscle hypertrophy ▪ Angiogenesis ▪ Inflammation

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