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Chronic Obstructive Pulmonary Disease, Hypertension and Osteoarthritis - Coursework Example

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The paper "Chronic Obstructive Pulmonary Disease, Hypertension and Osteoarthritis" states that in 2012 COPD was ranked the 5th leading cause of death while hypertensive diseases ranked at number 18. COPD, osteoarthritis and hypertension show a high prevalence among older adults aged above 65 years…
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Case Study: COPD, Hypertension and Osteoarthritis Student’s Name Institutional Affiliation Case Study: COPD, Hypertension and Osteoarthritis The presentation of a given medical condition largely informs a comprehensive assessment and documentation of findings (Brown & Edwards, 2011). Conditions such as obstructive pulmonary disease (COPD) and hypertension comprise a significant disease burden in the Australian population just like in other parts of the world (Australia Institute of Wealth and Welfare [AIHW], 2012; Australian Centre for Asthma Monitoring [ACAM], 2011). For instance, in 2012 COPD was ranked the fifth leading cause of death while hypertensive diseases ranked at number 18 (Australian Bureau of Statistics [ABS], 2014). COPD, osteoarthritis and hypertension show a high prevalence among older adults aged above 65 years (Brown & Edwards, 2011). This paper shall examine the pathophysiology and related pharmacological management of the symptomatic presentation of the three conditions as they present in Nancy. In addition, a prioritised plan of care for the patient shall be discussed with a focus on aspects of nursing care, ongoing assessment, the interdisciplinary team and the patient education. Pathophysiology of COPD COPD is a substantially irreversible medical condition that is primarily caused by exposure to cigarette smoke for a long time, and it progresses insidiously. It is estimated that over 90% of COPD cases are as a result of chronic tobacco smoking, including Nancy's (MacNee, 2005). Pathophysiology of COPD arises from three main processes that include protease-antiprotease imbalance, oxidative stress and airway inflammation that combine to give the symptomatic features of COPD (MacNee, 2006). Cigarette smoke contains several chemicals that can irritate the epithelial lining of the respiratory tract. Epithelial irritation results in the stimulation and increased release of inflammatory cells such as neutrophils (MacNee, 2006). As these inflammatory cells are continuously secreted, a more than standard inflammatory process ensues with the cells secreting reactive oxidant species and proteases that potentially deform lung capillaries (MacNee, 2006). In addition, cigarette smoke also activates other inflammatory cells such as macrophages and T-lymphocytes chiefly the CD8+ type. The inflammatory cells secrete cytokines that orchestrate a continuous lung and airway deformation and destruction (Brashier & Kodgule, 2012). Serum proteinases including neutrophil elastases and proteinases such as matrix metalloproteinase (MMP) 8 and 9 are secreted by neutrophils and they progressively cause insidious alveolar destruction, excess mucous secretion and accumulation in both small and large airways potentially blocking the former and narrowing the lumen of the large airways consequently obstructing airflow (Tuder & Petrache, 2012). Perforins and granzymes released by CD8+ T cells cause apoptotic death of alveoli epithelial cells leading to emphysema as experienced by Nancy. Damaged alveoli impair gaseous exchange in the alveoli due to reduced alveoli number and surface are of gas exchange. The result is a ventilation-perfusion mismatch, impaired oxygenation of blood and excretion of carbon dioxide lowering the partial pressure of oxygen SpO2 in blood as it was observed in Nancy, and increasing the SpCO2 in blood. Impaired oxygenation results in tissue hypoxia that presents as cyanosis as seen on Nancy's lips that had turned blue. Repeated inflammation induces the release of pro-fibrotic inflammatory mediators such as TGF-beta that cause airway fibrosis that progressively results in fixed airway narrowing (Brashier & Kodgule, 2012). This enhances airways resistance further limiting ventilation. In addition, the stiffened narrowed airways cause reduced airflow especially in the course of expiration and greatly audible breathing as observed with Nancy (Brashier & Kodgule, 2012). Obstructed breathing and impaired gaseous exchange due to alveoli destruction stimulates the respiratory centre to increase the work of breathing, increase the respiratory rate and engage the accessory muscles of respiration, presenting as a bulge in Nancy’s neck and shoulder muscles, in an attempt to improve ventilation in the lungs (Brown & Edwards, 2011). Damage to the epithelium also impairs the adaptive and innate immune response increasing the susceptibility to infections (MacNee, 2006). This may explain why Nancy has an infection and why she might be prone to more frequent episodes of respiratory tract infections. The initially elevated temperature and thick sputum are attributable to the infection (MacNee, 2006). The poor lung function and wellbeing can be depressing for the patient if she does not understand the disease including its prognosis and feels hopeless about it. Pathophysiology of Hypertension Hypertension is an elevation in blood pressure (BP) defined as diastolic and systolic pressure above or equal to 90mmHg and 140mmHg respectively or if a patient is on drugs that manage high BP (AIHW, 2012). It progresses in three phases starting with prehypertension with systolic BP range of 120-139 and diastolic range of 80-89, stage 1with systolic BP ranging between 140-159 and a diastolic range of between 90-99, and later stage 2 hypertension with systolic BP of at least 160 and diastolic of at least 100 when control of BP is not done or if its done insufficiently (Brown & Edwards, 2011). Nancy’s hypertension is associated with her advanced age of 68 years coupled with other risk factors such as alcohol consumption and tobacco smoking (Fleg & Strait, 2011). Ageing is associated with functional and structural arterial changes. Among the structural changes include arterial wall hypertrophy and increased deposition of materials such as calcium and extracellular matrix (Fleg & Strait, 2011). Increased synthesis and release of vasoconstrictors such as endothelins and decreased secretion of vasodilators such as nitric oxide comprise functional changes that impairs the distensibility of arteries. The stiff, difficult-to-dilate and narrowed lumen of arteries raises “arterial systolic and pulse pressure” and increases the heart’s workload (Fleg & Strait, 2011). This is manifested in Nancy who has a relatively higher systolic BP (over 140) compared to diastolic BP (less than 80), and since the afterload is increased too, the heart is working extra hard exhibited by the increased heart rate at 104 beats/minute. Pathophysiology of Osteoarthritis Osteoarthritis, also common in individuals with advanced age, is a hugely noninflammatory condition characterised by degenerative changes in the synovial joints especially the articular cartilage, subchondral bone, and synovial fluid (Vincent K, Conrad, Fregly & Vincent, H., 2012). As individuals advance in age, the repair and regeneration of tissue becomes suboptimal. Therefore, damage to the joint's hyaline cartilage or exposure to excessive load results in poor healing as the chondrocytes ability to repair the worn out cartilage through the synthesis of proteoglycans is weakened. Eventually, softening of the cartilage and loss of elasticity occurs comprising the integrity of the joint surface, causing erosion of cartilage and loss of joint space consequently exposing the underlying bone. When the underlying bone is exposed, friction during movements along these bone surfaces results in pain, and it progressively impairs movement as experienced by Nancy (Vincent et al., 2012). In addition, the vascular invasion response of the subchondral bone results in vascular congestion causing an increase in intraosseous pressure perceived as pain by the patient (Lozada, 2015). The pain and limitation in movement can be depressing to the patient, as observed in Nancy’s due to inability to perform various activities of daily living independently (ADL). Pharmacological Management The pharmacological management of the three main conditions affecting Nancy entails the use of a variety of medicines targeting different physiological activities to relieve the symptoms experienced by the patient. Management of COPD Pharmacological management of COPD entails the use of drugs such as bronchodilators. The latter have a salient role in decreasing the tone of airway smooth muscles, improving the flow of air in the airways, and limiting hyperinflation (O’Donnell et al., 2008). The result is a relief in dyspnoea and improved ability to cope with physical activity. Bronchodilator use is guided by the severity of COPD assessable via spirometry. They include beta 2 agonists and antimuscarinics. Beta 2 agonists are dived into short acting (SA) and long-acting (LA) agents. Nancy is on a short acting agent – salbutamol. They act on airways beta 2 adrenergic receptors resulting in relaxation of airways smooth muscles and consequently, bronchodilation (Evensen, 2010). Therefore, they improve airflow obstruction enhancing the movement of air into and out of the lungs. If a sustained improvement in ventilation is required, LA agents such as formoterol may be used to support the SA agents (O’Donnell et al., 2008). The latter has been demonstrated to reduce the frequency of exacerbations of COPD Anticholinergic form another class of bronchodilators. They inhibit acetylcholine mediated increase in bronchomotor tone, hence, inhibit vagally mediated bronchoconstriction (Evensen, 2010). For instance, Nancy is on ipratropium, an antimuscarinic agent used in the maintenance control of bronchospasm. In addition, she is also on tiotropium, an antimuscarinic that has been shown to improve dyspnoea, lung function and quality of life (O’Donnell et al., 2008). Tiotropium also has sustained bronchodilator effect, thereby, relieving the airways obstruction hence keeping the patient free of breathing difficulties (Evensen, 2010). Oral corticosteroids are essential to Nancy during this time when she is experiencing an exacerbation of COPD. They possess an anti-inflammatory effect that is significant in reducing the inflammatory effect on the bronchioles and airways, reducing secretions such as mucus and sputum from the inflammatory cells that would otherwise aggravate respiratory tract obstruction and worsen difficulties in breathing (O’Donnell et al., 2008). Although not all patient exhibit response to prednisolone, an oral corticosteroid, a short-term oral dose can reduce the duration of hospital stay during an exacerbation (O'Donnell et al., 2008). Due to a damaged respiratory epithelium, the susceptibility to respiratory infections is increased. This necessitates the use of antibiotics such as the Amoxicillin that Nancy has been prescribed for empirical management and prevention of multiplication of bacteria colonising the respiratory tract and their dissemination into the bloodstream that may result in severe infection before culture and sensitivity results are available for more specific antimicrobial therapy (Evensen, 2011). Management of Hypertension Blood pressure is a result of the product of peripheral vascular resistance (PVR) and cardiac output (CO). PVR is increased in Nancy, and it’s attributable to the increased arterial tone associated with ageing aggravated by cigarette smoking and alcohol consumptions as risk factors. The pharmacological antihypertensive target the reduction of either PVR, CO or both. Nancy has her BP elevated to very high levels at 170/90. The use of medication such as furosemide, a diuretic, enhances urinary sodium loss that is accompanied by water loss consequently leading to blood volume decrease and less CO (Brown & Edwards, 2014). A decline in the latter results in a cumulative reduction in BP. Since Furosemide alone may not sufficiently reduce the BP, other antihypertensive agents such as "angiotensin converting enzyme inhibitors [ACEI]" are significant too. ACEI include perindopril arginine that aid in the reduction of PVR by inhibiting angiotensin II-mediated increase in vascular tone and blood volume (Nelson, 2010). ACEI also lowers the risk of cardiovascular-related morbidity that the patient is at risk of given her age and existing hypertension (Nelson, 2010). The result of ACEI therapy is a decrease in both CO and PVR leading to a decrease in BP that would also relieve the patient’s comfort and anxiety regarding a bad premonition. Management of Osteoarthritis Osteoarthritis has no known cure, and most of the pharmacological management measures are geared at relieving pain and improving the functionality of the patient (Lozada, 2015). Osteoarthritis pain hinders or limits the patient's movement limits physical activity increasing the risk factors for deterioration in her wellbeing. A sustained release version of paracetamol branded as Panadol Osteo has been prescribed to the patient. It contains a higher paracetamol dose (665 mg) compared to the regular paracetamol hence providing the much needed sustained relief from osteoarthritic pain (GlaxosmithKline, 2015). Prioritised Plan of Care Prioritization of care shall be based on the ABCDE pneumonic where priority shall be given to first level priority life-threatening conditions affecting the patient’s “airway, then breathing, circulation, disability, and exposure” (Thim, Krarup, Grove, Rohde & Lofgren, 2012). Nancy is experiencing airways obstruction caused by the COPD exacerbation evident by the increase in breathing effort and noisy breathing. Therefore, prescribed bronchodilator therapy will be administered starting with ipratropium administered through an inhaler. The patient shall be assisted to actuate and inhale the medicine as prescribed. Other bronchodilator pharmacological agents are due for administration shall also be administered to avert the risk of respiratory obstruction (Lozada, 2015). Nancy's breathing shall be the next aspect to given consideration. From the physical examination findings such as blue coloured lips and the pulse oximetry results, she has insufficient breathing with poor oxygenation of blood leading to tissue hypoxia. Therefore, the administration of oxygen therapy shall be continued while monitoring for improvement in tissue oxygenation or disappearance of cyanosis signs. Circulation assessment findings indicate an elevation in BP. The patient is a known hypertensive hence her BP should be controlled by administering the prescribed antihypertensive medication. The patient is alert and oriented without identifiable risk of deterioration of disability status. Routine assessment of these parameters is necessary in assessment and monitoring the patient’s progress after initial management measures. The patient will require review by a medical officer incorporating the changes in management prescribed by the GP. After prioritization of the above needs, the other second level priority patient needs shall be attended to (White, Duncan & Baumle, 2011). The patient is in pain related to her osteoarthritis. The limbs and her body shall be positioned in postures that do not strain the joints in addition to a routine change in position. Furthermore, pain relieving medication due for administration shall be administered. Bed and sitting positions shall be monitored as she is at risk of falls. Her special dietary requirements require consultation or referral to a dietician as she is underweight with dysphagia limiting intake of some solid oral meals (Brown & Edward, 2014). Nutritional review notes and recommendations made by the dietician shall be incorporated in the management of the patient’s nutritional status. Patient education is instrumental in enhancing the patient’s self-efficacy in taking control of his health. This includes providing the necessary reading materials regarding the conditions, rights of the patient and their carer, educating on the need to adhere to prescribed Drug and Alcohol service instructions to maintain abstinence from cigarette smoking even while admitted to the hospital, and educating on relaxation techniques including vision activities and manual imagination to help alleviate the psychological stress caused by the conditions (Delui, Yari, Khouyinezhad, Amini & Bayazi, 2013). The patient education also involves orientation and introduction to hospital routines such as ward routine, meal times and visiting hours. Conclusion Appropriate management of a patient’s medical condition requires an understanding of the pathophysiological presentation of the conditions some of which age is a risk factor. Individuals whose age has advanced such as Nancy are at risk of comorbidities such as COPD, hypertension and osteoarthritis. Their management should be holistic with the relevant specialists consulted and incorporated. Conditions such as COPD predominantly affect the respiratory tract affecting the ventilation and blood oxygenation, areas that should be given priority during management before attending to other less life-threatening conditions such as the mild osteoarthritic pain and the poor patient’s nutritional status. Apart from the pharmacological management, non-pharmacological therapy such as patient education, heat and cold, occupational and physical therapy are significant especially in management of osteoarthritis (Lozada, 2015). References Australian Bureau of Statistics. (2014). Causes of death, Australia, 2012. Retrieved from http://www.abs.gov.au/ausstats/abs@.nsf/Lookup/3303.0main+features100012012 Australian Center for Asthma Monitoring. (2011). Asthma in Australia 2011: with a focus chapter on chronic obstructive pulmonary disease. Canberra: AIHW. Australian Institute of Health and Welfare. (2012). Australia's health. Canberra: AIHW. Brashier, B.B. & Kodgule, R. (2012). Risk factors and pathophysiology of chronic obstructive pulmonary disease (COPD). Journal of Association of Physician of India, 60, 17-21. Brown, D. & Edwards, H. (2011). Lewis's medical-surgical Nursing: Assessment and management of clinical problems (3rd ed.). Chatswood, NSW: Mosby Australia. Delui, M.H., Yari, M., Khouyinezhad, G. & Bayazi, M.H. (2013). Comparison of cardiac rehabilitation programs combined with relaxation and meditation technique for reduction of depression and anxiety of cardiovascular patients. Open Cardiovascular Medical Surgery, 7, 99-103. Evenson, A.E. (2010). Management of COPD exacerbations. American Family Physician, 81(5), 607-613. Fleg, J.L. & Strait, J. (2011). Age-associated changes in cardiovascular structure and function: A milieu for future disease. Heart Failure Review, 17, 545-554. Glaxosmithkline. (2015). Panadol Osteo (paracetamol). Retrieved from https://www.gsk.com.au/products_consumer-healthcare-products_detail.aspx?view=90 Lozada, J.C. (2015). Osteoarthritis. Retrieved from http://emedicine.medscape.com/article/330487-overview#a0104 MacNee, W. (2006). Pathogenesis of chronic obstructive pulmonary disease. Proceedings of the American Thoracic Society, 2, 258-256. Nelson, M. (2010). Drug treatment of elevated blood pressure. Australian Prescriber, 33, 108-112. O'Donnell, D.E., Hernandez, P., Kaplan, A., Aaron, S., Bourbeau, J., Marciniuk, D., ... & Voduc, N. (2008). Canadian thoracic society recommendations for management of chronic obstructive pulmonary disease - 2008 update- highlights for primary care. Canadian Respiratory Journal, 15(Suppl A), 1a-8a. Thim, T., Hrarup, N.H.V., Grove, E.L., Rohde, C.V. & Lofgren, B. (2012). Initial assessment and treatment with the airway, breathing, circulation, disability, exposure (ABCDE) approach. International Journal of General Medicine, 5, 117-121. Tuder, R.M. & Petrache, L. (2012). Pathogenesis of chronic obstructive pulmonary disease. The Journal of Clinical Investigation, 122(8), 2749-2755. Vincent, K.R., Conrad, B.P., Fregly, B.J. & Vincent, H.K. (2012). The pathophysiology of osteoarthritis: A mechanical perspective on the knee joint. Physical Medicine and Rehabilitation Journal, 4(5 Suppl), S3-S9. White, L., Duncan, G. & Blaumle, W. (2011). Foundations of basic nursing (3rd ed.). Clifton Park, NY: Delmar, Cengage Learning. Yoshida, T. & Tuder, R.M. (2007). Pathophysiology of cigarette smoke-induced chronic obstructive pulmonary disease. Physiological Reviews, 87(3), 1047-1082. Read More
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