This assignment will discuss the pathophysiology of a disease process of chronic obstructive pulmonary disease (COPD). It will also show how biological, psychological and the social aspects of the disease that can have an affect on an individual’s day to day life. COPD stands for chronic obstructive pulmonary disease. This is a term used for a number of conditions; including chronic bronchitis and emphysema.
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COPD leads to damaged airways in the lungs, causing them to become narrower and making it harder for air to get in and out of the lungs. The word ‘chronic’ means that the problem is long-term. COPD is a condition which mainly affects people over the age of 40, and COPD has a higher prevalence occurring among women than men (NHS-Choices, 2008). COPD is also a condition that is long term and incurable that can have a serious affects on health and quality of life, its not fully understood why COPD develops. (Marieb, 2003). The student will also incorporate local and national health and social policies, including frameworks that are in place in relation to the patients illness. The student identified a patient named Mrs J. She was admitted to hospital due to exacerbation of COPD. Her primary diagnosis is Osteoarthritis of the Hip but also had symptoms of emphysema. Mrs J is a 55 year old women and is married, Mrs J also has an older child whom she has become quite dependant on and felt like she had impacted on her child’s life and had become a hindrances. Mrs J has become more breathless as her condition develops over time and more so while she was lying in bed unable to carry out her daily activities such as doing the housework, leisure activities, also looking after her appearance as she normally would have done at home. COPD is becoming one of the fastest leading causes of disability (NHS choices, 2008). According to British Lung Foundation, (2010) a recent survey, 83% of COPD patients said their COPD slows them down, 79% said they had to cut down their activities and 56% said their condition has a great affect on their families. COPD is the most common respiratory conditions in adults in the developed world and poses an enormous burden to society both in terms of direct cost to the healthcare services and indirect costs to society through loss of productivity. Recent analysis estimated that National Health Service (NHS) spends £818 million annually in the United Kingdom (UK). (British Thoracic Society, 2006). However 50% of the cost is accounted for by poorly managed exacerbations resulting in frequent re-admissions to hospital (Coakley & Ruston, 2001).
Mrs J condition would of been triggered by her heavy smoking, the toxins from her cigarettes has made her bronchioles (airway and lungs) become inflamed and narrowing the airway, this will lead to irreversible damage to the respiratory system by obstructing the bronchial airflow and hindering gaseous exchange within the alveoli (Munden, J, 2007). Mrs J suffers from many symptoms due to her smoking these include shortness of breath, a persistent cough, yellowish green sputum, signs of cyanosis to her lips, also Mrs J has continued to smoke as she thinks the damage has already been done so her condition. The vast majority of COPD patients are smokers. By stopping smoking patients can slow the rate of decline in lung function and thus improve the patient’s prospects in terms of symptoms and survival.
The National Institute of Clinical Excellence guidance on COPD states that “All patients still smoking, regardless of age, should be encouraged to stop, and offered help to do so, at every opportunity.”
These deliver a small dose of medicine to the lungs, causing the airway muscles to open up. Bronchodilators are also effective in preventing over-expansion of the lungs. Short-acting beta2-agonists are the most commonly used short acting bronchodilaors for COPD. Their effects last for about 4 hours. Short-acting antichloinergics are also used as bronchodilators.
Long-acting beta2-agonists are similar to the short-acting agonists described above but their effect lasts for 12 hours.
Lomg-acting anti-cholinergics need only be taken once a day.
The NICE guidance recommends that short-acting bronchodilators should be used for the initial treatment for breathlessness and exercise limitation and goes on to say that, if this isn’t having an effect then the treatment should be intensified using eith er a long-acting bronchodilator or a combined therapy with a short acting beta2-agonist and a short-acting anticholinergic
The respiratory system is the major part for gases exchange to take place, it allows takes the air that enters are bodies when we inhale and travels through the respiratory system, exchanging oxygen for carbon dioxide and expels carbon dioxide when we exhale (munden, J, 2007). In the NHS there is a tool to calculate the smoking load and the packs in a year this tool is called smoking pack tool, this was used to see the damage that Mrs J had caused by smoking for so many years.
This is because the seriousness of the disease depends on how much and how long the individual has smoked for.
Mrs J has been smoking now for 45 years and on a average day having up to 40 cigarettes a day and is not prepared to quit as she feels the damage is already done. Mrs J smokes for comfort and feels that its all for her pleasure, she has become very isolated, her chronic bronchitis makes her breathless when doing actives and is not able to do her daily activities therefore is becoming depressed. Do this having a huge impact on her mental and social parts of her life.
Patients with COPD have traditionally been divided into pink puffers and blue bloaters based on their physiological response to abnormal blood gases. The former work hard to maintain a normal pO2 which is why they puff away. They tend to have a barrel-shaped, hyperinflated chest and breath through pursed lips. The latter are blue because of hypoxia and polycythaemia. They are often obese and have water retention. This is why they are bloated. The blue bloaters are dependent upon hypoxia for their respiratory drive and to give oxygen and deprive them of this will lead to signficant hypercapnia and acid base imbalance. Although this concept is widely taught and acknowledged academically, in clinical practice patients tend not to be clearly in one or the other of these two categories (NICE Clinical Guideline (2004)
Patients like Mrs J with airflow limitation clinically they have become known as ‘pink puffers’ and ‘blue bloaters’ (Kleinschmidt, 2008). Mrs J falls under the term ‘blue bloaters’ as she linked to chronic bronchitis due to cyanosis which is a blue tinge to the lips, which occurs from poor gas exchange.
‘pink puffers’ has been linked to emphysema as the patients may be showing signs of weight loss, using their accessory muscles with pursed lips giving them a reddish complexion, they may also adopt the tripod sitting position (Kleinschmidt, 2008). Although these conditions separate the patient may present with slight variations of them both, however they do differentiate through their underlying process, signs and symptoms (Bellamy & Booker, 2004).
Airways and air sacs within the lungs are manly elastic, with the air we breath the lungs change shape with inhalation they expand and return to the normal shape after they have been stretched with air.
Mucociliary clearance is an important primary innate defense mechanism that protects the lungs from deleterious effects of inhaled pollutants, allergens, and pathogens. Mucociliary dysfunction is a common feature of chronic airway diseases in humans. The mucociliary apparatus consists of three functional compartments, that is, the cilia, a protective mucus layer, and an airway surface liquid (ASL) layer, which work in concert to remove inhaled particles from the lung.
The nose and nasal cavity are composed of ciliated columnar epithelium cells which contain goblet cells and cilia, the goblet cells are responsible for secreting mucus which is able to trap the finer particles from inspired air and the cilia which are fine hairs that can trap larger particles. The cilia carry’s the particles by a sweeping motion this is swept to the mouth or nose where it can then be swallowed, coughed or sneezed out of the body in order to prevent these particles from entering the lungs (Munden, J, 2007).
The two major sources of mucus secretion in the respiratory tract are the surface epithelial goblet cells and mucous cells. In lungs, goblet cells are present in the large bronchi, becoming increasingly thin toward the bronchioles. The submucosal glands are restricted to the large airways with their density decreasing with airway calibre. In chronic respiratory diseases, such as COPD and asthma, submucosal glands increase in size (hypertrophy), and the number of goblet cells is increased (hyperplasia), becoming more dense in the peripheral airways, via a phenotypic conversion of nongoblet epithelial cells (metaplasia) (Rogers, 1994;Jackson, 2001). The increased of goblet cells density to ciliated cells in the bronchioles, under the conditions of hypersecretion, this impairs clearance of mucus.
Lung histology from patients affected by COPD and asthma also shows the presence of edema, which can further reduce airway caliber and compromise lung function. A marked airway infiltration of macrophages and granulocytes is also present, principally neutrophils in COPD and eosinophils in asthma (Postma and Kerstjens, 1998). In clinical studies, these inflammatory parameters have been shown to correlate with a reduction in lung function (FEV1) and an exaggerated bronchoconstriction [airway hyperreactivity (AHR)] to nonspecific stimuli (Postma and Kerstjens, 1998). Smoking has many effects on the airways. Inhaled smoke destroys the cilia that are important for moving mucus to the throat for swallowing. As a result, mucus accumulates in the bronchioles and irritates the sensitive tissues there, causing a cough. Coughing is vital as it is the only way smokers can remove mucus from their lungs and keep the airways clean (Rubin, 2002). This is characterised by the ‘smoker’s cough’.
Constant coughing to clear the sputum has an effect on the smooth muscle of the bronchioles which becomes hypertrophied (enlarged or overgrown). This in turn causes more mucus glands to develop.
The goblet cells are replaced within the small airways (bronchi) with Clara cells they are another form of secreting cell these are important they form ciliated cells and to help regenerate the bronchiolar epithelium, they produce hypophase component and a protease inhibitor these help protect the lungs by mopping up debris (Stokley et al, 2006).To accomplish gas exchange the lung has two components; airways and the alveoli. The airways are two branching tubular passages that allow air to move in and out of the lungs, the wider segments of the airways are called the trachea and the two bronchi going to the right and left lung. The smaller segments are called the bronchioles and at the end of the bronchioles are the alveoli which are thin walled sacs like a bunch of grapes; small blood vessels (capillaries) run in the walls of the alveoli this is where gas exchange between air and blood takes place. (Matterporth & Matfin, 2009).
Rogers, 1994;Jackson, 2001
Chronic obstructive pulmonary disease, NICE Clinical Guideline (2004); Management of chronic obstructive pulmonary disease in adults in primary and secondary care
COPD. BMJ Clinical Evidence. www.clinicalevidence.com, accessed 10 June 2009
Textbook of Medical Physiology (10th edition)
Guyton, A.C. and Hall, J.E. (2000) W.B. Saunders, Philadelphia; London.
Global Initiative for Chronic Obstructive Lung Disease; September 2005.
Britton M; The burden of COPD in the U.K.: results from the Confronting COPD survey.; Respir Med.2003 Mar;97 Suppl C:S71-9. [abstract]
Chronic obstructive pulmonary disease, NICE Clinical Guideline (2004); Management of chronic obstructive pulmonary disease in adults in primary and secondary care
Lacasse Y, Goldstein R, Lasserson TJ, et al; Pulmonary rehabilitation for chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2006 Oct 18;(4):CD003793. [abstract]
Barr RG, Bourbeau J, Camargo CA, et al; Inhaled tiotropium for stable chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2005 Apr 18;(2):CD002876
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