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Asthma - Risk Factors, Airflow Limitation in Asthmatic Patients, Drug Therapy for Chronic Asthma - Case Study Example

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The paper “Asthma - Risk Factors, Airflow Limitation in Asthmatic Patients, Drug Therapy for Chronic Asthma” is an affecting example of a case study on nursing. Asthma is a persistent condition characterized by prevalent, erratic, and reversible airflow difficulty, which is either impulsive or pharmacologically stimulated…
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Asthma Case Study Name: Instructor: Course: Institution: Date: Asthma Case Study Question 1 Asthma is a persistent condition characterized by prevalent, erratic, and reversible airflow difficulty, which is either impulsive or pharmacologically stimulated. The causal pathophysiological characteristic of asthma is increased airway responsiveness, which develops on a basis of diffuse bronchial inflation. Episodes may happen impulsively or in reaction to various factors including respiratory diseases, psychological trauma, or changes in weather conditions. Asthma usually worsens at night, with studies on nocturnal asthma indicating that there is a circadian and sleep-related variation in hormones and respiratory function, with airway narrowing because of bronchospasm, edema of the bronchial mucosa, and mucus plugging (Porth & Matfin 2010, p.576). A mild touch may produce a feeling of chest tightening, slight increase in respiratory rate with prolonged expiration and mild or loud wheezing. Coughing is an important physiologic mechanism to clear the airway of debris to allow better ventilation and prevent infection. Factors influencing coughing may be results from irritation of the airways, vocal cords from inflammation, or infection, among other causes. This may also result from anatomic injuries to chest wall musculature, ribs, or the lungs themselves. In addition to these causes of cough, it may also result from fatigue and sleep deprivation. (Brown 2003, p.74). The most common causes of chronic cough include postnatal drip with or without sinusitis, gastroesophageal reflux, and cough variant asthma. The reasons for cough in pathophysiology of asthma are primarily airway inflation and irritation, although mucus overproduction contributes significantly in some patients. In this regard, shortness of breathing may last for several hours and consists of progressive deepening of breaths. This may result from the mild hypoxia caused by fatigue of the respiratory center and nervousness, associated with stressful stimuli (Brown 2003, p.73). Two genetic influences identified with pathophysiology of asthma include the ability of an individual to develop asthma (atopy) and tendency to develop hyper-responsiveness of the airways independent of atopy. A section of chromosome 11 related to atopy includes an unusual genetic material that predetermines section of the immunoglobulin (Ig) E receptor. Environmental characteristics related with hereditary characteristics to give rise to asthma related to bronchospams. In asthmatic individuals, bronchial covering responds to various causative factors, which leads to spasms in the smooth muscle and further, reduce the size of airways. On successive antigen exposure, degranulation of mast cells occurs releasing mediators. As a result, this causes interstitium’s mast cells to produce leukotrienes and histamine (Marone 1998). The resulting Histamine embeds to larger bronchi’s receptors leading to inflammation of muscle walls. Mucous membranes become inflated, irritated, and swollen, causing the individual to have protracted exhaustion, increased rate of breathing and dyspnea. On the other hand, Leukotrienes embed to the smaller bronchi’s receptors, leading to bulging of smooth muscle. Leukotrienes also cause prostaglandins to travel through the bloodstream to the lungs, where they enhance histamine’s effect. Wheezing may become louder when the patient is coughing, an indication of continued narrowing of bronchial lumen. Histamine stimulates the mucous membranes to secrete viscous mucus that is difficult to cough up, resulting in coughing, rhonchi, increased-pitch wheezing, and increased respiratory distress, mucosal edema and thickened secretions further block the airways (Murphy, 2007). Question 2 Some of the risk factors that may have been in Anna’s house include: (i) Allergens - Exposure of asthmatic individuals to allergic substances remains a causative factor for asthma and/or the persistence of its symptoms. The exposure of asthmatic individuals to allergens increases bronchial hyper-responsiveness. Allergens in Anna’s house may have included dust and fur of the pet animals she kept in her house (Murphy 2007). (ii) Tobacco smoking - In the house, there might have existed or had an occurrence of tobacco smoking among the members, which on exposure leads to increase in severity of asthma, decreasing response to treatment, and influencing decrease in lung functions. (iii) Indoor air pollution- Such factors as smoke and fumes, use of solid-cooking fuels (biomass fuels) and poor ventilation might have been some of the risk factor in Anna’s house. These are believed to cause breathing difficulties in asthmatic patients (Murphy 2007). (iv) Extreme emotional expression- Emotions trigger asthma exacerbations, primarily because they can lead to hyperventilation and hypocapnia, which can cause airway narrowing. Panic episodes, which are uncommon but not extraordinary in some asthmatic individuals, have a comparable consequence. In addition, psychological traumatic events may be essential causal factors that may contribute recurrence of asthma. They can also lead to morbidity in asthmatic condition through causing neuroimmunologic actions to activate exacerbations. Since it was Anna’s birthday, some of these factors, including excessive laughter, surprises, exhaustion, among others may have been present, thereby causing Ruby’s condition to worsen (Brown 2003). (v) Other risk factors that might have been present include sudden changes in temperature and weather, food additives, colorings, and flavorings. Question 3 “Forced vital capacity (FVC) and forced expiratory volume in one second (FEV1)” are used for the assessment of airflow limitation and in useful screening of early airflow limitation in asthmatic patients and subsequent management of people with COPD (Thiadens et al. 1999, p.1055). They serve an essential role in managing and evaluating prognosis particularly in assessing disease severity in lung functions. FVE1 is a ‘good standard’ in the measurement of airway narrowing and is a component of the severity scores in guidelines from the National Asthma Education and Prevention Program. Variation in airflow limitation is commonly tested by measuring the response of FEV1 to an inhaled bronchodilator. In addition, daily recording of peak expiratory flows rates can be used to assess variability in lung functions. Also in respect to airways hyper-responsiveness, an exaggerated response to the bronchoconstrictor can be observed. Thus, FVC remains a valuable PFT indicator for assessing cases of obtrusive pathology in asthmatic patients. It is a responsive measure for the incidence of obtrusive airway ailment through using FEV1. If a person’s FEV1 falls below the anticipated FEV1, then the person can be said to have a form of obstructive ailment in the lungs. Question 4 From the results, FEV1 = 950ml and FVC = 2300ml Therefore; Ruby’s FEV1/FVC ratio = 950ml/2300ml = 0.41 Since 0.41< 0.7, it indicates that Ruby has an obstructive disease (Aggarwal, Gupta, & Jindal 2006). Question 5 Drugs likely to be in ‘reliever’ inhaler include bronchodilator medications, such as terbutaline and salbutamol, which exist in a variety of brand names. Commonly, these drugs have bluish color and taken to relieve signs of breathlessness, chest tightness, and wheezing. On the other hand, medications likely to be present in ‘preventer’ inhaler primarily comprise of steroid drugs, which are taken daily to avert irritations and swellings in the airways. Although there are a variety of steroid medicines in the market today, the commonly used include fluticasone, budesonide, mometasone, ciclesonide, and beclometasone (Patient UK 2010). Question 6 Relievers are short-acting bronchodilators that work by relaxing the muscles that have tightened around the airways. They open up the airways quickly, implying that they are used only when needed to ease the patient breathing. Preventers are long-term medicines taken every day, usually over long periods, to control chronic symptoms and to prevent asthma episodes or attacks. They slowly reduce the sensitivity the patient has towards irritants and allergens that would normally trigger an attack and relieve airway constriction for a long period (about 12 hours). Drugs that relieve bronchoconstriction act either to stimulate β2 adrenoceptors, to block cholinergic receptors on the membranes of bronchial smooth muscle cells (Anderson & Thomas 2010). β2-adrenergic agonists activate these receptors causing an increase in cyclic AMP in the cell cytoplasm, which triggers muscle relaxation. They release a chemical, called acetylcholine, onto the smooth muscle cells within their walls, causing them to contract. As a result, the airways narrows and stops acetylcholine from stimulating the smooth muscle and encourages the airways to relax again. It lowers the viscosity of purulent and non-purulent pulmonary secretion by breaking the disulfide linkages in pulmonary mucus secretion (Kadam 2008, p.293). Vasoconstriction of nasal capiliary bed is brought about by activation of local α-adrenergic receptors. Vasoconstriction of engorged nasal mucosa allows the inhibition of vascular leakage, drainage of sinuses, and clearing of airways. Question 7 Ruby’s arterial pH was lower than the normal since the normal total lungs capacity (TLC) and the normal gases diffusion were low. This was due to low FEV1/FVC ratio, which, according to Mehrotra et al. (2009), is commonly associated with obstruction, hyperinflation, air trapping, and impairment in gas transportation from the air to blood. Therefore, due to a low FEV1/FVC rate, an elevated total lung capacity (TLC) and reduced diffusion of gases creates smaller lung volumes and impairment to gas exchange, consequently lowering the pH. Question 8 Yes, Ruby could as well tell the doctors about her asthma and her medication in order to avoid incidences of medical errors. Usually, it is useful for patients to inform doctors (if not their personal doctors) about medications that they have been using in order for the doctors to determine the correct drugs and dosage. Otherwise, the physicians may be forced to assume various issues which may greatly harm or cause death of the patients due to medical errors. References Aggarwal, AN, Gupta, D, & Jindal, SK 2006, ‘The relationship between FEV1 and peak expiratory flow in patients with airways obstruction is poor,’ Chest, vol.130, no. 5, pp.1454-1461. Anderson, M & Thomas DA 2010, ‘Drug therapy for chronic asthma in children,’ ADC Education & Practice Edition, vol. 95, no. 5, pp. 145-150. Brown, ES 2003, Asthma: social and psychological factors and psychosomatic syndromes, Karger Publishers, Basel. Inhalers for asthma 2010, Patient UK, viewed on 10 Feb 2010, Kadam, SS 2008, Principles of medical chemistry: vol. 1, Pragati Books Pvt. Ltd, New Delhi Marone, G 1998, Asthma and allergic diseases: physiology, immunopharmacology, and treatment. Academic Press, San Diego, CA. Mehrotra, R, Bross, R, Wang, H, Appell, M, Tso, L, & Kopple JD 2009, ‘Effect of high-normal compared with low-normal arterial PH on protein balances in automated peritoneal dialysis patients,’ American Journal of Clinical Nutrition, vol. 90, no. 6, pp. 1532-1540. Murphy, A 2007, Asthma in focus, Pharmaceutical Press, London. Porth, CM & Matfin, G 2010, Essentials of pathophysiology: concepts of altered health states, 3rd edn., Lippincott Williams & Wilkins, Baltimore, MD. Thiadens, HA, De Bock, GH, Van Houwelingen, JC, Dekker, FW, De Waal, MW, Pringer, MP, & Postma, DS 1999, ‘Can peak expiratory flow measurements reliably identify the presence of airway obstruction and bronchodilator response as assessed by FEV1 in primary care patients presenting with a persistent cough?’, Thorax, vol. 54, no. 12, pp. 1055-1060. Read More
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