ANSWERS TO THE ASSESSMENT QUESTIONS 1
Answersto the Assessment Questions
Asthma is a heterogeneous disease in connection with clinicalphenotype, immunopathology, therapy response as well as historicalnature. The severity of asthma symptoms is controlled byenvironmental factors or are caused by the insufficientanti-inflammatory treatment (Marshall and Biensenstock, 1994).Therefore, the clinical dimension of asthma has a high variability ofairway inflammation as a consistent dimension. The inflammationpatterns in asthma is connected with AHR (clinically measured byhistamine or methacholine challenge) which results in frequentincidence of breathlessness, wheezing, tightness of chest andcoughing especially at night and in the morning. These incidences aregenerally connected to obstruction within the lungs that are mostlyreversible either with treatment or spontaneously. in mostasthmatics, inflammation is mostly limited to the conducting airways,although, with an increase in disease severity, the inflammatoryinfiltrate to the small airways as well as adjacent alveoli, in somecase (Homer, 1997). T-lymphocytes has a critical role in theorganization of the inflammatory counter in asthma. The release of,prostaglandins and cytokines, specific patterns of inflammatorymediators leads to the integration and endurance of eosinophils andin the sustenance of mast cells in the airways.
Cytokines areproteins that act as chemical messengers and have been recognized toregulate the development, growth or activity of target cells bybinding to specific receptors on their surface. Chemokines are asub-group of cytokines involved in chemotaxis, they are critical forcell migration during routine immune surveillance, inflammation anddevelopment of activities. Cytokines are produced as a response to atrigger and various inflammatory cytokines mediate the systemiceffects. Nevertheless, the overproduction of inflammatory cytokineshas a significant contribution to some symptoms of a severinginflammatory illness like asthma and rheumatoid arthritis. Most ofthe inflammatory cells such as the mast cells have the ability tosynthesize and release these proteins. Besides, structural cells likeASM cells have been recognized to produce a variety of cytokines,subsequently playing a role in the inflammatory response.
Another pathogenesisof asthma is the response to triggers such as exercise and allergicsensitization the airways recognize common triggers and in turnproduce a Th2 kind of cytokine reaction to them. Asthma is also foundto involve vascular, mesenchymal, local epithelial and neurologicactions, which lead the Th2 lymphocytes to the lung. Repeated boutsof increased inflammation in asthma may lead to damage of the airwayepithelium, and subsequent abnormal repair leads to structuralchanges in the airway walls of asthmatic subjects. There isrecruitment and activation of leukocytes in response to the trigger.Following activation, the cells work actively to neutralize theantigens, subsequently they repair any damage finally, the cells areremoved by resolution of the inflammatory process.
Once an asthmaexacerbation has been recognized, immediate intervention needs to beput in place so as to improve the hypoxia, bronchoconstriction, andinflammation. The main strategies of intervention available for nurseinclude oxygen administration and inhaled beta2-agonists (Barnett etal., 1997). The dose incidence and route of administration for theserelies on patient assessment and response to treatment. Oxygensaturation should be obtained on all children to assess the level ofhypoxia. Although children appear to have normal oxygenation uponphysical examination, they often can be hypoxemia. Therefore,respiratory distress and documented hypoxemia are the common factorsdetermining when oxygen is required. The nurse can use various cutoffpoints between 90-95%. Besides when the child is receiving oxygentherapy, it is not necessary to maintain a SaO2 greaterthan 92% through oxygen concentration because of the potential foralveolar collapse and resulting atelectasis and increased hypoxemia.
Inhaledbets2-agonists are recommended as a first-line pharmacologicintervention for all children for the treatment ofbronchoconstriction, regardless of asthma severity (Kelly and Murphy,1992). Albuterol is the most common beta2-agonist provided.Continuous delivery has an advantage over intermittent in thatcontinuous treatment decreases the risk for undertreatment, mayimprove PEFR better than intermittent treatment and decreases thelength of stay in the emergency department. Metered-Dose inhalers,dry powder inhalers or nebulizers are equally effective inbeta-agonist delivery. The mode of beta2-agonist delivery mightdepend on the age of the child as well as the level of distress.
Ipratropiumcontains an ammonium group that prevents systematic absorption. Theydo this by preventing the effects of acetylcholine on airways as wellas nasal passages. In response to a trigger, the cholinergic nervesin the lungs cause the airways to be narrow by triggering thecontraction of bronchi surrounding the muscle (Beck et al, 1997).Ipratropium is an anticholinergic drug that prevents the effect ofcholinergic nerve leading to the relaxation of muscles and dilationof airways. Also, ipratropium helps to prevent the symptoms of coldby blocking the secretion of mucus in the nose. This is accomplishedby blocking acetylcholine.
When anticholinergicmedication is added to salbutamol, there isadditional bronchodilation, improved PEFRs, and decreased emergencydepartment stay period. Salbutamol is a selective beta2-agonist withpowerful bronchodilator effect. It achieves this by reducingbranchiomotor tone. It is recognized that stimulation ofbeta2-receptors triggers the stimulation of cyclic adenosinemonophosphate via conversion of ATP by adenyl cyclase (Becket al., 1997). The cyclic adenosine monophosphate thenstimulates a chain of intracellular events that produce thephysiologic effect. The stimulated beta2 receptor relaxes the smoothmuscle around the bronchi within 3- 15 minutes. Since the action isso rapid, salbutamol is prescribed for immediate relief of symptomswhenever the need arise.
When these drugs areinhaled at suggested dosage, the have fairly few side effects owingto their selectivity. However, a portion of the inhaled drug isinexorably absorbed into the systematic circulation (Larsen, 1992).High dosage of these drugs may lead to elevated heart rate, centralnervous system, and cardiac arrhythmias effects related withbeta-adrenergic activation such as restlessness. The currentrecommendation demands the provision of salbutamol more than threetimes a week 200-1000ug per day of beclomethasone-chlorofluorocarbonfor children. This represents the next stage in the continuum wheresymptom characteristic are considered persistent, and the severity ofasthma is rated moderate or worse. When acceptable control isachieved, the goal of management is to establish the minimal amountof medication needed to maintain symptom control. Regular follow-upand re-evaluation of the treatment regimen is critical to asthmamanagement. This includes the creation of an action plan, doing anevaluation of environmental control, confirmation that compliancewith medication is maintained, continuing education and if demanded,specialist referral.
Barnett, P.L.J., Caputo, G.L., Baskin, M. & Kuppermann, N.(1997). Intravenous versus oral corticosteroids in the management ofacute asthma in children. Pediatrics, 29 (2), 212-217.
Beck, R., Robertson, C, Galdes-Sabaldt, M.R., & Levison, H.(1985). Combined salbutamol and ipratropium bromide by inhalation inthe treatment of acute severe asthma. Journal of Pediatrics. 107.605-608.
Homer, C.J. (1997). Asthma disease management. The New EnglandJournal of Medicine. 337 (20): 1461-1463.
Kelly, H.W. & Murphy, S. (1992). Beta-adrenergic agonists foracute, severe asthma. Annals of Pharmacotherapv. 26. 81-91.
Larsen, G.L. (1992). Asthma in children. New England Journal ofMedicine. 326. 1540-1550.
Marshall, J.S., & Biensenstock, J. (1994). The role of mast cellsin inflammatory reactions of the airways, skin and intestine.Current Opinion in Immunology. 6. 853-859.