This project will discuss the pathophysiology of the disease procedure persistent obstructive lung illness (COPD). It will take a look at how this illness affects an individual looking at the biological, psychological and social elements. It will achieve this by describing a patient who was confessed to a medical ward with an exacerbation of COPD.
Additionally with support of Gibbs model of reflection (as pointed out in Bulman & & Schutz, 2004) it will show how an experience changed a mindset. In accordance with the Nursing and Midwifery Council, (NMC) Code of Expert Conduct (NMC, 2005) regarding securing patient information no names or places will be disclosed.
For that reason throughout the assignment the client will be referred to as John. John is a 57 years of age gentleman who has actually been married to Mavis for two years. John was confessed to the ward with extreme breathlessness cough and extreme sputum production. By browsing John’s notes it was discovered this was an exacerbation of COPD.
To understand John’s condition it works to look at how the typical breathing system works. The function of the breathing System is to supply the body with oxygen and eliminate carbon dioxide (Marieb, 2004). According to Waugh and Grant (2004) it also helps preserve body temperature and get rid of excess water from the body. The Respiratory system includes the mouth, nasal cavity, throat, larynx, trachea, bronchi and the lungs (Seeley, Stephens & & Tate, 2000). Air enters through either the mouth or nose which humidifies and cleans up the air.
(Cohen & & Wood, 2000) combining into a typical chamber called the oropharynx (Watson, 2000). Air then delegates the vocal cords, a short, funnel-shaped tube that transports air to the larynx (Waugh & & Grant, 2004). The air gets in the larynx which is lined with mucous membrane and continues to the trachea, which is formed of semi-circular cartilage rings. The inner membrane of the trachea includes hair cells and mucous cells which trap particles and sweeps them towards the bronchi. The bronchi are also lined with mucous membrane and ringed with cartilage (Marieb, 2004).
Each bronchus is lined with mucous membrane. (Martini, 2000) and extends into a lung where it subdivides forming smaller bronchioles (Watson, 2000). Bronchioles terminate with the alveoli which are the functional units for gas exchange and are thin, moist and surrounded by capillaries (Clancy & McVicar 2001). Inhaled air travels through these airways to the alveoli. Blood is pumped out of the heart through the pulmonary arteries to the capillaries surrounding the alveoli. (Shaw, 2005) The oxygen of the inhaled air diffuses out of the alveoli into the blood, while carbon dioxide in the blood moves into the alveoli to be exhaled (Tortora & Grabowskie, 2003). The oxygen-rich blood is returned to the heart through the pulmonary veins.
The lungs can expand and contract without friction during breathing due to the pleura, a thin membranous structure (Tamir, 2002). The visceral pleura surround the lungs, while the parietal pleura line the wall of the thoracic cavity. These pleura are separated by a small fluid-filled space called the pleural cavity. Ventilation requires work and before the lungs can become inflated, a pressure change must take place. The elastic properties of the lung allow ventilation to take place more efficiently and the fluid in the pleural cavity serves as a lubricant that allows the lungs to slide against the chest wall (Marieb, 2004).
John notified the staff that he was diagnosed with COPD twelve months ago by his general practitioner (G.P.). He added that he repeatedly went to his G.P. as he had been feeling breathless, which was becoming worse and was present every day, more so when he exercised. This breathlessness he revealed was accompanied by a cough alongside sputum production. John’s G.P inquired if he smoked and how many, John informed him he has smoked around 30 cigarettes a day for 42 years. The doctor then gave John a lung function test using a spirometer. John was notified by his GP that he had COPD which, John was informed, was both chronic bronchitis and emphysema (National Lung Health Education Program, 2005).
The World Health Organization (WHO) (2006A) defines COPD as a disease state characterized by airflow limitation that is not wholly reversible. The airflow limitation is usually both progressive and associated with abnormal inflammatory response of the lungs to noxious particles or gases. John’s chronic bronchitis is defined, clinically, as the presence of a chronic productive cough for 3 months in each of 2 successive years, provided other causes of chronic cough have been ruled out. (Mannino, 2003). The British lung Foundation (BLF) (2005) announces that chronic bronchitis is the inflammation and eventual scarring of the lining of the bronchial tubes which is the explanation for John’s dyspnea. The BLF (2005) believe that when the bronchi become inflamed less air is able to flow to and from the lungs and once the bronchial tubes have been irritated over a long period of time, excessive mucus is produced. This increased sputum results from an increase in the size and number of goblet cells (Jeffery, 2001) resulting in John’s excessive mucus production. The lining of the bronchial tubes becomes thickened and an irritating cough develops, (Waugh & Grant 2004) which is an additional symptoms that john is experiencing.
Emphysema affects the parenchyma of the lung through destruction of the alveolar walls, leading to permanent enlargement of air spaces distal to the terminal bronchioles (Sandford, Weir & Pare, 1997). The walls between adjacent alveoli break down, the alveoli ducts dilate and there is loss of interstitial elastic tissue (Watson, 2000) This results in distention of the lungs and loss of normal elastic recoil, therefore trapping and stagnation of alveolar air (National Emphysema Foundation, 2006). As alveoli merge there is loss of surface area for gaseous exchange (Alexander, Fawcett & Runciman, 2004) resulting in less oxygen. This loss of area for gaseous exchange is an additional explanation for John’s dyspnea.
John was referred to the physiotherapist to help alleviate his breathlessness and mucus production. Turner Foster & Johnson (2005) pronounce physiotherapists are key members of the intervention team, can education and give John practical guidance on how he can breathe comfortably and effectively. (United Kingdom Parliament, 2005). Van der Schans, Postma, Koeter & Rubin (1999) suggest physiotherapists facilitate John’s mucus transport by using breathing techniques, percussion and postural drainage. Moreover they can educate John on body positioning as this is fundamental with people with COPD (Gosselink, 2003).
Additionally John was referred to the Occupational Therapist (OT) who assessed his current level of fitness and then formulated a program of activities which will improve his overall strength and stamina. The OT can also give advice to John to manage his condition with the least distress and disruption of daily living (Turner Foster & Johnson 2005). Furthermore the National Institute of Health and Clinical Excellence (NICE) (2004) recommend patient with COPD should be regularly asked about their ability to undertake activities of daily living and how breathless they become when doing these.
John was informed that his COPD was possibly caused by smoking. Kanner (1996) believes that the major environmental factor of COPD is tobacco smoke. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) (2005) concurs and states cigarette smoking is by far the most important risk factor for COPD. This according to the National Heart Blood and Lung Institute (NHLBI) (2006) is because smoking irritates the lungs, which causes the airways to become inflamed and narrowed. Additionally Verra, Escudier, Lebargy, Bernaudin, De Cremoux & Bignon (1995) adds that enzymes released because of the inflammation breaks down elastin, the protein important for structural integrity of the lungs, creating breathing air in and out of the lungs more difficult (NHLBI, 2006)
However D’hulst, Maes, Bracke, Demedts, Tournoy, Joos & Brusselle (2005) states not all smokers develop clinically significant COPD, which suggests that genetic factors must modify each individual’s risk (WHO, 2006B). John continues to smoke although he has reduced his intake; however NICE (2004) guidelines suggest all COPD patents who continue to smoke should be encouraged to stop, and offered help to do so, at every opportunity because, smoking cessation is the single most effective way to reduce the risk of developing COPD and stop its progression (WHO, 2006B). John was encouraged to stop, given guidance on how to stop, was informed about a smoking cessation group that he could attend and in addition offered nicotine patches; however he refused and told staff that he would quit in his own time.
John explained to the nurse that for the past few months he has been feeling low, can not concentrate and has a lack of interest in anything, he says he does not understand why he is feeling this way. Gross (2001) believes these symptoms could be a sign of depression. According to Kunik, Roundy, Veazey, Souchek, Richardson, Wray & Stanley (2005) many CODP patients develop psychological symptoms in addition to physical complaints. According to Kunik & Densmore (2002) this is because of the nature of the disease and the fear of being breathless. The BLF (2005) concur and believe breathing difficulty can instigate anxiety and depression. Other causes stated by Ohri & Steiner (2004) include body image, increased loneliness, lack of social support, and low self-esteem. Kunik et al (2005) report that depression and anxiety are two to three times more prevalent in COPD patients than in the general population and the explanation for this is because of the sustained and persistent feelings of frustration, hopelessness and helplessness.
John’s depressed mood could lower his level of energy needed to cope with his chronic illness, which, in turn, could make his symptoms less tolerable. (Singer, Ruchinskas, Riley, Broshek & Barth, 2001) Depression also can lead to increased severity of John’s medical symptoms since feelings of depression can cause a person to be less active, and, in turn, may exacerbate physical deterioration, which can intensify the psychosocially crippling effects of COPD (Van Ede, Yzermans & Brouwer, 1999). However a study by Engstrom, Persson, Larsson, Ryden & Sullivan (1996) found that quality of life is not significantly affected in patients with mild to moderate COPD, possibly due to coping and/or pulmonary reserve capacity.
John was given the opportunity to talk to a psychiatrist since mental health specialist can diagnose depression and provide appropriate treatment. One treatment that was suggested was pulmonary rehabilitation. Mahler (1998) states these programs incorporate psychosocial and behavioral components. Emery, Leatherman, Burker & MacIntyre (1991) agree and suggests that it can also enhance cognitive functioning and psychological well-being. Studies by Withers, Rudkin & White (1999) reiterate this and show that levels of anxiety and depression were significantly enhanced by pulmonary rehabilitation.
John was 56 when he was diagnosed with COPD. He stated he was forced to take early retirement from his employment where he assisted in the repair, installation and maintenance of water and sewer lines. This, he believes was because of the time lost at work caused by his dyspnea. Mavis declared she also had to resign from her part time job as a cleaner to take care of John since she is his only carer and is exhausted. Their income is from government benefits and a small pension and they say they are finding it difficult to manage on the amount of money they receive. Strassels, Smith, Sullivan, & Mahajan (1987) reported that the typical COPD patient was more than 65 years old and had limited work loss directly related to his or her disease. However a study by Tinkelman & Corsello (2003) indicated that COPD is not just a disease of the elderly. They state a large percentage of patients with COPD are unable to work, and those who do work miss days as a result of their disease. This situation they believe is of great concern to the individual worker who may lose his job as a consequence of excessive absenteeism.
Chronic illness and disability are strongly class related (Taylor & Field 1993) and those in the lower socio-economic groups are the most affected. Smoking, the greatest risk factor for COPD and exposure to occupational factors from manual unskilled jobs, such as mining and foundry working are highest amongst males in the lower socio-economic groups (Parnell, 2000). COPD patients and their families tend to be members of this group and are often elderly as symptoms become intrusive in the fifth and sixth decades of life which is John’s situation. Webb & Tossell (1999) maintain that pensions often reflect an individual’s class and social status and as a result more women, retired manual workers and ethnic minorities are disproportionately represented in old age as being on the margins of poverty.
A reliance on state benefits may be a consequence if forced to retire early and carers may not be entitled to benefits in their own right. The financial burden is increased by the costs of disability such as home alterations and help in the home or transport (Young, 1995). To help John and Mavis a social worker was involved who assisted with home care help when John was discharged so Mavis could have some time for herself. Additionally the OT was involved and provided equipment to help John maintain his independence (Trombly & Radomski 2000).
Although I was conscious, through study, other health professionals and through nurse training, that smoking can be detrimental to health and can cause diseases such as cancer (Newcomb & Carbone 1992) atherosclerotic diseases (McBride, 1992) and COPD (British Thoracic Society, 1997) I was unwilling to give health promotion and smoking cessation advice since I smoke myself. Several studies show that I am not alone in this thinking. Studies by Dore & Hoey (1998) and Adriaanse, Van Reek, Zandbelt & Evers (1991) show that high smoking rates among some populations of nurses may diminish their willingness and effectiveness as potential providers of smoking cessation care. An additional study by Nardini, Bertoletti, Rastelli , Ravelli & Donner (1998) demonstrated that smoking habits influence the attitude of health staff toward patient counseling about tobacco smoking. I considered that it was not my place and felt hypocritical if I attempted to give advice on stopping smoking. On meeting John my feelings did not change despite the fact that I could see the effects that COPD had on John’s breathing.
However on spending time with John and Mavis my attitude altered. I realized that if John stopped smoking then his condition, although his lost lung function would not be regained, (Booker, 2005) will be slowed down (Osman & Hyland, 2005). I became aware of the fact that I was in a prime position to aid John in maintaining his independence, to educate and to help improve John’s quality of life through health promoting and advice on smoking cessation. Although John decided not to give up this did not deter me on giving health promotion advice on smoking. On talking to other patients I took the opportunity to talk about stopping smoking although I did not do this aggressively (Seedhouse, 2004). This experience with John changed my feelings regarding health promotion and smoking. Although I still feel somewhat hypocritical, I acknowledge the importance of my position and how it can facilitate patients and their lives. I believe I understand the difficulties patients face when attempting to quit, perhaps more than a lifelong non smoker. I will continue to provide smoking cessation advice throughout my training and also throughout my career.
In conclusion this assignment has explained the pathophysiology of COPD through introducing a patient. It examined how this individual has been affected holistically. Finally it demonstrated how an experience encountered altered an opinion with help from a reflective model.