Pathophysiology of copd essay

This job will explain the pathophysiology of the disease process long-term obstructive pulmonary disease (COPD). It will take a look at how this kind of disease affects an individual taking a look at the natural, psychological and social aspects. It will make this happen by discussing a patient who had been admitted into a medical ward with a great exacerbation of COPD. Furthermore with assistance of Gibbs model of representation (as cited in Bulman & Schutz, 2004) it will eventually demonstrate just how an experience altered an attitude. In accordance with the Medical and Midwifery Council, (NMC) Code of Professional Perform (NMC, 2005) regarding shielding patient data no labels or spots will be divulged.

Therefore through the assignment the sufferer will be termed as John. Ruben is a 57 year old gentleman who has recently been married to Mavis for 2 years. Steve was confessed to the ward with severe breathlessness coughing and increased sputum creation. By looking through John’s notes it was found out this was a great exacerbation of COPD.

To comprehend John’s state it is helpful to look at the way the normal breathing works.

The function of the breathing is to give you the body with oxygen and remove carbon (Marieb, 2004). According to Waugh and Grant (2004) it also helps maintain body temperature and eliminate excess drinking water from the human body. The Respiratory system consists of the mouth, nasal cavity, pharynx, larynx, trachea, bronchi and the lung area (Seeley, Stephens & Tate, 2000). Atmosphere enters through either the mouth or nostril which humidifies and wipes the air. (Cohen & Wooden, 2000) merging into a prevalent chamber referred to as the oropharynx (Watson, 2000). Air then simply leaves towards the pharynx, a brief, funnel-shaped conduit that carries air to the larynx (Waugh & Give, 2004). The air enters the larynx which is lined with mucous membrane and takings to the trachea, which is produced of semi-circular cartilage bands. The inner membrane layer of the trachea contains frizzy hair cells and mucous cells which pitfall particles and sweeps these people toward the bronchi. The bronchi are also lined with mucous membrane layer and ringed with the fibrous connective tissue cartilage (Marieb, 2004).

Each bronchus is covered with mucous membrane. (Martini, 2000) and extends right into a lung in which it subdivides forming smaller sized bronchioles (Watson, 2000). Bronchioles terminate with the alveoli the functional models for gas exchange and are thin, wet and surrounded by capillaries (Clancy & McVicar 2001). Inhaled air trips through theseairways to the alveoli. Blood is usually pumped out of your heart through the pulmonary arterial blood vessels to the capillary vessels surrounding the alveoli. (Shaw, 2005) The oxygen with the inhaled atmosphere diffuses out of the alveoli in to the blood, when carbon dioxide in the blood goes 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 increase and agreement without friction during breathing as a result of pleura, a skinny membranous framework (Tamir, 2002). The pasional pleura encompass the lungs, while the parietal pleura collection the wall structure of the thoracic cavity. These pleura happen to be separated with a small fluid-filled space known as the pleural cavity. Fresh air requires job and before the lungs can become inflated, a pressure change must occur. The flexible properties from the lung enable ventilation to happen more efficiently as well as the fluid inside the pleural tooth cavity serves as a lubricant that permits the lung area to slip against the breasts wall (Marieb, 2004).

Ruben notified employees that having been diagnosed with COPD twelve months back by his general practitioner (G. P. ). He added that this individual repeatedly visited his G. P. as he had been sense breathless, that has been becoming more serious and was present every day, more so if he exercised. This breathlessness he revealed was accompanied by a cough alongside sputum production. John’s G. P inquired in the event he smoked cigarettes and how a large number of, John informed him he has smoked around 35 cigarettes per day for 42 years. The doctor then gave John a lung function test utilizing a spirometer. John was informed by his GP that he had COPD which, John was educated, was the two chronic bronchitis and emphysema (National Lung Health Education Program, 2005).

The World Overall health Organization (WHO) (2006A) defines COPD as a disease express characterized by air flow limitation which is not wholly invertible. The air flow limitation is normally both intensifying and linked to abnormal inflammatory response from the lungs to noxious particles or gas. John’s long-term bronchitis is definitely defined, medically, as arsenic intoxication a long-term productive cough for 3 months in each of 2 successive years, presented other reasons for chronic cough have been ruled out. (Mannino, 2003). The English lung Groundwork (BLF) (2005) announces that chronic bronchitis is the inflammation and final scarring of the lining from the bronchial tubeswhich is the reason for John’s dyspnea. The BLF (2005) believe that if the bronchi become inflamed fewer air is able to flow to and from the lung area and once the bronchial pipes have been inflammed over a lengthy period of time, increased mucus is produced. This kind of increased sputum results from a rise in the size and number of goblet cells (Jeffery, 2001) leading to John’s increased mucus creation. The lining from the bronchial tubes becomes thickened and an irritating coughing develops, (Waugh & Give 2004) which can be an additional symptoms that ruben is encountering.

Emphysema affects the parenchyma of the chest through destruction of the alveolar walls, leading to permanent growth of air flow spaces distal to the terminal bronchioles (Sandford, Weir & Pare, 1997). The walls between adjacent alveoli break down, the alveoli system dilate and there is loss of interstitial elastic tissue (Watson, 2000) This brings about distention from the lungs and loss of usual elastic recoil, therefore trapping and wachstumsstillstand of unaccented air (National Emphysema Base, 2006). Because alveoli merge there is loss of surface area to get gaseous exchange (Alexander, Fawcett & Runciman, 2004) leading to less o2. This decrease of area for gaseous exchange is yet another explanation to get John’s dyspnea.

John was referred to the physiotherapist to aid alleviate his breathlessness and mucus development. Turner Create & Meeks (2005) pronounce physiotherapists will be key people of the intervention team, may education and provide John useful guidance on just how he can inhale and exhale comfortably and effectively. (United Kingdom Parliament, 2005). Vehicle der Schans, Postma, Koeter & Rubin (1999) suggest physiotherapists assist in John’s nasal mucus transport through the use of breathing methods, percussion and postural draining. Moreover they can educate John on body positioning because fundamental with people with COPD (Gosselink, 2003).

Additionally Steve was labeled the Occupational Therapist (OT) who examined his current level of fitness then formulated a plan of actions which will improve his overall strength and stamina. The OT may also give guidance to Ruben to manage his condition with the least problems and disruption of everyday living (Turner Engender & Johnson 2005). Furthermore the Nationwide Institute of Health and Specialized medical Excellence (NICE) (2004) advise patient with COPD ought to beregularly mentioned their capacity to undertake actions of everyday living and how breathless they become when doing these.

Steve was informed that his COPD was possibly caused by smoking. Kanner (1996) is convinced that the major environmental aspect of COPD is cigarettes smoke. A global Initiative for Chronic Obstructive Lung Disease (GOLD) (2005) concurs and states smoking is by far the most important risk element for COPD. This in line with the National Cardiovascular system Blood and Lung Institute (NHLBI) (2006) is because smoking irritates the lungs, which in turn causes the airways to become swollen and concentrated. Additionally Verra, Escudier, Lebargy, Bernaudin, Sobre Cremoux & Bignon (1995) adds that enzymes produced because of the irritation breaks down elastin, the proteins important for strength integrity in the lungs, creating breathing surroundings in and out with 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 implies that innate factors must modify every individual’s risk (WHO, 2006B). John continues to smoke even though he has reduced his intake; nevertheless NICE (2004) guidelines suggest all COPD patents who continue to smoke cigarettes should be prompted to stop, and offered help to accomplish this, at every option because, smoking cessation is the single best approach to reduce the chance of developing COPD and stop its progression (WHO, 2006B). Steve was encouraged to stop, provided guidance on how to stop, was informed with regards to a smoking ukase group that he could attend and moreover offered pure nicotine patches; nevertheless he rejected and told staff that he would stop in his personal time.

David explained to the nurse that for the past several months he has been feeling low, can not put emphasis and has a lack of affinity for anything, he says he does not understand why he can feeling this way. Gross (2001) believes these kinds of symptoms may well 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 problems. According to Kunik & Densmore (2002) this is because with the nature with the disease plus the fear of getting breathless. The BLF (2005) concur and believe breathing difficulty can instigate anxiousness and major depression. Other triggers stated by Ohri& Steiner (2004) incorporate body image, elevated loneliness, lack of social support, and low self-pride. Kunik ainsi que al (2005) report that depression and anxiety will be two to three instances more prevalent in COPD sufferers than in the typical population and the explanation with this is because of the sustained and persistent feelings of frustration, pessimism and helplessness.

John’s frustrated mood can lower his level of strength needed to handle his serious illness, which in turn, in turn, might make his symptoms less bearable. (Singer, Ruchinskas, Riley, Broshek & Barth, 2001) Depression also can bring about increased severity of John’s medical symptoms since emotions of depression can cause a person to get less lively, and, subsequently, may exacerbate physical degeneration, which can heighten the psychosocially crippling associated with COPD (Van Ede, Yzermans & Brouwer, 1999). Even so a study by Engstrom, Persson, Larsson, Ryden & Sullivan (1996) identified that quality lifestyle is not significantly afflicted in patients with mild to modest COPD, possibly due to coping and/or pulmonary reserve capacity.

John was given the opportunity to speak to a professional since mental health specialist can diagnose major depression and provide appropriate treatment. One treatment that was recommended was pulmonary rehabilitation. Mahler (1998) declares these programs incorporate psychological and behavioral components. Emery, Leatherman, Burker & MacIntyre (1991) acknowledge and suggests that it can also boost cognitive performing and emotional well-being. Research by Withers, Rudkin & White (1999) reiterate this kind of and show that levels of anxiety and despression symptoms were considerably enhanced by pulmonary therapy.

John was 56 if he was clinically determined to have COPD. He stated he was forced to have early old age from his employment where he assisted inside the repair, unit installation and repair of water and sewer lines. This, he believes was because of the time lost at work caused by his dyspnea. Mavis declared in addition, she had to resign from her part time job as a solution to take care of Steve since she is his only carer and is also exhausted. Their particular income is definitely from authorities benefits and a small pension check and they say they are finding hard to manage within the amount of money they receive. Strassels, Smith, Sullivan, & Mahajan (1987) reported that the typical COPD patient was morethan 65 years of age and had limited work damage directly linked to his or her disease. However a report by Tinkelman & Corsello (2003) indicated that COPD is not just a disease of the elderly. They point out a large percentage of individuals with COPD are unable to job, and those whom do work miss days as a result of their disease. This situation they believe is of wonderful concern for the individual member of staff who may possibly lose his job as a consequence of excessive absenteeism.

Chronic health issues and incapacity are strongly class related (Taylor & Field 1993) and those in the lower socio-economic groups are the most affected. Smoking, the highest risk factor for COPD and experience of occupational elements from manual unskilled jobs, such as exploration and foundry working will be highest between males in the lower socio-economic groups (Parnell, 2000). COPD patients and their families are likely to be associates of this group and are typically elderly as symptoms become intrusive in the fifth and sixth many years of life which is John’s situation. Webb & Tossell (1999) maintain that pensions often reveal an individual’s class and cultural status and as a result more women, retired manual workers and ethnic minorities will be disproportionately represented in retirement years as being around the margins of poverty.

A reliance upon state rewards may be a consequence if required to retire early on and carers may not be qualified for benefits in their own right. The economic burden is usually increased by the costs of disability such as home alterations and help in your home or travel (Young, 1995). To help John and Mavis a cultural worker was involved who assisted with home care help when ever John was discharged and so Mavis would have some time to get herself. And also the OT was involved and provided products to help Ruben maintain his independence (Trombly & Radomski 2000).

Even though I was mindful, through study, other health professionals and through nurse teaching, that smoking can be detrimental to health and may cause diseases such as cancer (Newcomb & Carbone 1992) atherosclerotic diseases (McBride, 1992) and COPD (British Thoracic Culture, 1997) I used to be unwilling to offer health campaign and smoking cessation suggestions since I smoke myself. Several studies show that I was not alone with this thinking. Research by Dore & Hoey (1998) and Adriaanse, Vehicle Reek, Zandbelt & Evers (1991) demonstrate that substantial smoking rates among a few populations of nurses may possibly diminish all their willingness and effectiveness as potential providers ofsmoking ukase care. An additional study simply by Nardini, Bertoletti, Rastelli, Ravelli & Conférer (1998) demonstrated that smoking practices influence the attitude of health personnel toward sufferer counseling regarding tobacco smoking. I actually considered that it was not my place and felt hypocritical if I attempted to give guidance on blocking smoking. About meeting Ruben my feelings did not alter despite the fact that I could see the results that COPD had in John’s inhaling and exhaling.

However about spending time with John and Mavis my attitude changed. I realized that if David stopped smoking then his condition, although his shed lung function would not end up being regained, (Booker, 2005) will be slowed down (Osman & Hyland, 2005). I became mindful of the fact that I was in a first-rate position to aid John in maintaining his self-reliance, to educate and also to help improve John’s quality of life through health advertising and tips on cigarette smoking cessation. Though John didn’t give up this kind of did not prevent me upon giving wellness promotion tips on smoking cigarettes. On speaking with other individuals I required the opportunity to discuss stopping smoking cigarettes although Some do this strongly (Seedhouse, 2004). This experience of John transformed my emotions regarding well being promotion and smoking. Although I continue to feel relatively hypocritical, My spouse and i acknowledge the value of my position and how it can assist in patients and the lives. I think I understand the down sides patients deal with when attempting to quit, perhaps more than a ongoing non person. I will still provide smoking cessation tips throughout my personal training and also throughout my own career.

In conclusion this job has explained the pathophysiology of COPD through presenting a patient. This examined how this individual has been affected holistically. Finally that demonstrated how an experience experienced altered an impression with help from a reflective unit.

References

Alexander, M. N., Fawcett, L. M., & Runciman, G. J. (Eds. ). (2004). Nursing practice hospital and home ” The adult (2nd impotence. ). Edinburgh: Churchill Livingstone.

Adriaanse, H., Van Reek, J., Zandbelt, L., & Evers, G. (1991). Nurses’ smoking throughout the world. A review of 73 surveys in nurses’ cigarettes consumption in 21 countries in the period 1959-1988. Intercontinental Journal of Nursing Studies, 28, 361-375.

Booker, 3rd there’s r. (2005). Long-term obstructive pulmonary disease and nice suggestions. Nursing regular, 19(22).

Uk Lung Groundwork (2005). COPD. Retrieved March 14, 2006, from http://www.lunguk.org/copd.aspBritish Thoracic Contemporary society (1997). BTS guidelines to get the administration of chronic obstructive pulmonary disease. Torso, 52(5).

Bulman, C., & Scultz, S. (2004). Refractive practice in nursing (3rd ed. ). Oxford: Blackwell.

Clancy, L., & McVicar, A. (2001). Physiology and anatomy: a homeostatic procedure (2nd education. ). London: Arnold.

Cohen, B. T., & Real wood, D. L. (2000). Memmler’s the human body in health and disease (9th male impotence. ). Phila.: Lippincott Williams & Wilkins.

D’hulst, A., Maes, T., Bracke, K., Demedts, M Tournoy, K., Joos G., & Brusselle G. (2005). Cigarette smoke-induced pulmonary emphysema in scid-mice is the obtained immune system needed?. Respiratory Analysis, 6(147).

Dore, K., & Hoey, L. (1998). Smoking cigarettes practices, know-how and attitudes regarding smoking of university hospital nurses. Canadian Journal of Public Health, 4(79).

Emery, At the. F., Leatherman, N. Electronic., Burke, At the. J., & MacIntyre, D. R. (1991). Psychological outcomes of a pulmonary rehabilitation system. American university of torso physicians, 42(7).

Engstrom, C., Persson, M., Larsson, S i9000., Ryden, A., & Sullivan, M. (1996). Functional position and well-being in serious obstructive pulmonary disease with regard to clinical variables and smoking cigarettes: a descriptive and relative study. Chest, 51(30).

Gosselink, R. (2003). Controlled deep breathing and dyspnea in individuals with serious obstructive pulmonary disease. Log of rehab research and development, 40(5).

Global Motivation for Serious Obstructive Chest Disease (2005). Global technique for the analysis, management, and prevention of chronic obstructive pulmonary disease. Retrieved Feb 19, 2006, from http://www.goldcopd.com/Guidelineitem.asp?l1=2&l2=1&intId=989Gross, R. (2001). Psychology: technology of brain and patterns (4th impotence. ). London: Hodder and Stoughton.

Jeffery, P. T. (2001). Remodeling in bronchial asthma and chronic obstructive chest disease. American Journal of Respiratory and Critical Attention Medicine, 164(28).

Kanner, 3rd there’s r. (1996). Early intervention in chronic obstructive pulmonary disease: a review of the lung health study effects. Medical Clinics of United states, 80(4).

Kunik, M., & Densmore, Deb. (2002). Major depression and COPD. Geriatrics, 7(4).

Kunik, Meters., Roundy, T., Veazey, C., Souchek, M., Richardson, P., Wray, And., & Stanley, M. (2005). Surprisingly excessive prevalence of anxiety and major depression in long-term breathing disorders. American university of breasts physicians, 127(4).

Mahler, G. A. (1998). Pulmonary treatment. Chest, 113(26).

Mannino, G. M. (2003). Chronic obstructive pulmonary disease: definition and epidemiology. Breathing care diary, 48(12).

Marieb, E. (2004). Human anatomy & physiology. Bay area: Pearson Education.

Martini, N. (2000). Basics of anatomy of human body. New Jersey:

Prentice-Hall.

McBride, P. Elizabeth. (1992). The health consequences of smoking. Heart problems. Medical Treatment centers of America, 76(2).

Nardini, S., Bertoletti, R., Rastelli, V., & Ravelli, M., & Donner, C. (1998). Personal smoking habit and attitude toward smoking among the list of health staff of a general hospital. Monaldi Archive for Chest disease, 53(1).

National Emphysema Groundwork (2006). COPD ” What exactly is it?. Retrieved Mar 11, 06\, from http://emphysemafoundation.org/copdcbro.jsp#COPDWhatNational Heart Blood and Chest Institute (2006). What Causes COPD?. Retrieved Drive 8, 2006, from http://www.nhlbi.nih.gov/health/dci/Diseases/Copd/Copd_Causes.htmlNational Institute for Health and Specialized medical Excellence (2004). Management of chronic obstructive pulmonary disease in adults in primary and secondary treatment. Retrieved February 12, 2006, from http://www.nice.org.uk/pdf/CG012_niceguideline.pdfNational Lung Overall health Education Plan (2005). Precisely what is COPD? Gathered March 19, 2006, via http://www.nlhep.org/lung_copd.htmlNewcomb, S. A., & Carbone, P. P. (1992). The health implications of smoking cigarettes: Cancer. Medical Clinics of North America, 76(2).

Nursing & Midwifery authorities. (2004). Code of professional conduct. Birmingham: Nursing & Midwifery authorities.

Ohri, C., & Steiner, M. (2004). COPD: the disease and non drug treatment. Medical center pharmacist, 14.

Osman, T. M., & Hyland, Meters. E. (2005). Patient requires and medication models in COPD. The Western european Respiratory World, 14(7).

Parnell, H. (2000). Respiratory disease: Caring for the carers of chronic chest disease sufferers in the community. Recovered February 23, 2006, coming from http://www.jcn.co.uk/journal.asp?MonthNum=05&YearNum=2001&Type=backissue&Arti

cleID=346Seedhouse, M. (2004). Health promotion: viewpoint, prejudice, and practice (2nd ed. ). Chichester: T. Wiley.

Seeley, R. Ur., Stephens, Big t. D., & Tate, L. (2000). Human anatomy (5th male impotence. ). UNITED STATES: McGraw- Mountain higher education.

Sandford, A. T., Weir, Capital t. D., & Pare, P. D. (1997). Genetic risk factors to get chronic obstructive pulmonary disease. European Respiratory Journal, 10(42).

Shaw, L. (2005). Anatomy and physiology. Cheltenham: Nelson ThornesSinger, L., Ruchinskas, 3rd there’s r., Riley, E., Broshek, Deb., & Barth, J. (2001). The psychological impact of end-stage chest disease. American college of chest medical professionals, 120(4).

Strassels, S. A., Smith, G. H., Sullivan, S. Deb., & Mahajan, P. (1987). The costs of treating COPD in the United States. American college of chest medical doctors, 119(9).

Tamir, E. (2002). The human body made simple: a guide to anatomy, physiology, and disease. Edinburgh: Churchill Livingstone.

Taylor, S i9000., & Field, D. (Eds. ). (1993). Sociology of health and medical: an introduction to get nurses (3rd ed. ). London: Blackwell Scientific Journals.

Tinkelman, O., & Corsello, P. (2003). Chronic obstructive pulmonary disease: the impact happens earlier than we believe. American Diary of Managed Care, 9(6).

Tortora, G. J., & Grabowski, S i9000. R. (2003). Principals of anatomy and physiology. Nyc: HarperCollins College or university Publishers.

Turner, A., Create, M., & Johnson, S i9000. E. (2005). The practice of occupational therapy: an intro to the remedying of physical problems (5th ed. ). Birmingham: Churchill Livingstone.

Trombly, C. A., & RadomskI, M. V. (Eds. ). (2000). Occupational therapy for physical dysfunction. Phila.: Lippincott Williams & Wilkins.

United Kingdom legislative house (2005). Memorandum by the Chartered Society of Physiotherapy. Gathered March being unfaithful, 2006, via http://www.publications.parliament.uk/pa/cm200506/cmselect/cmhealth/485/485we23.htmVan Ede, L., Yzermans, C. L., & Brouwer, H. L. (1999). Frequency of major depression in patients with persistent obstructive pulmonary disease: a systematic review. Torso, 17(4).

Van der Schans, C. L., Postma, M. S., Koeter, G. H., & Rubin, B. E. (1999). Physiotherapy and bronchial mucus travel. European Respiratory system Journal, 13(8).

Verra, F., Escudier, At the., Lebargy, Farreneheit., Bernaudin, J. F., Para Cremoux, H., & Bignon. J. (1995). Ciliary malocclusions in bronchial epithelium of smokers, ex- smokers, and nonsmokers. American Journal of Respiratory Critical Care Medication, 151.

Watson, R. (2000). Anatomy and physiology intended for nurses. Edinburgh: Bailliere Tindall.

Waugh, A., & Grant, A. (2004). Ross and Wilson human anatomy in health and health care. (9th ed. ). Edinburgh; Ny: Churchill Livingstone.

Webb, Ur., & Tossell, D. (1999). Social Problems for Carers: Towards Confident Practice (2nd ed. ). London: Arnold.

World Health Organization. (2006A). COPD: A definition. Retrieved February 21 years old, 2006, coming from http://www.who.int/respiratory/copd/definition/en/index.htmlWorld Wellness Organization. (2006B). COPD: Causes. Retrieved Feb 19, 06\, from http://www.who.int/respiratory/copd/causes/en/index.htmlWithers, N. L., Rudkin, S i9000. T., & White RJ, R. T. (1999). Anxiety and depressive disorder in serious

serious obstructive pulmonary disease: the effects of pulmonary rehabilitation. Journal of Cardiopulmonary Treatment, 19(6).

Young, P. (1995). Mastering cultural welfare (3rd ed. ). London: Macmillan Press.

1

Tweet