The pathophysiology of a disease: COPD

The pathophysiology of a illness COPDThis assign custodyt will discuss the pathophysiology of a disease process of chronic preventive pulmonary disease (COPD). It will besides show how biological, psychological and the social aspects of the disease that flock put up an put on on an individuals day to day life. COPD stands for chronic clogging pulmonary disease. This is a term employ for a number of conditions including chronic bronchitis and emphysema.COPD leads to injured shineways in the lungs, causing them to become narrower and making it hard-foughter for air travel to get in and expose of the lungs. The word chronic means that the problem is retentive-term. COPD is a condition which generally affects people oer the age of 40, and COPD has a higher prevalence occurring among women than men (NHS-Choices, 2008). COPD is too a condition that is long term and incurable that nominate restrain a serious affects on health and quality of life, its non fully understood why COPD develops. (Marieb, 2003). The student will also merged local and national health and social policies, including frameworks that ar in address 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 alone 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 dep destroyant on and felt like she had impacted on her childs life and had become a hindrances. Mrs J has become much inanimate as her condition develops over time and more so while she was lying in buns unable to carry out her daily activities such as doing the housework, unoccupied activities, also looking after her appearance as she normally would sire done at home. COPD is becoming one of the fastest leading causes of deterrent (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 healthc atomic number 18 services and confirmative costs to society through loss of productivity. Recent analysis estimated that subject Health Service (NHS) spends 818 million annually in the United body politic (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 gage, the toxins from her cigarettes has make her bronchioles ( air hose and lungs) become inflamed and narrowing the air hose, this will lead to irreversible damage to the respiratory system by obstr ucting the bronchial airflow and hindering vaporific exchange wi undersized the alveoli (Munden, J, 2007). Mrs J suffers from many symptoms due to her bullet these befool 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 repair the patients prospects in terms of symptoms and survival.The National Institute of Clinical Excellence focusing on COPD states that All patients still smoking, regardless of age, should be encouraged to stop, and offered servicing to do so, at every opportunity.These deliver a small window glass of medicine to the lungs, causing the airway muscles to open up. Bronchodilators are also potent in preventing over-expansion of the lungs. Short- playacting 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 exactly their effect lasts for 12 hours.Lomg-acting anti-cholinergics need only be taken one time a day.The NICE guidance recommends that short-acting bronchodilators should be used for the initial intervention for breathlessness and exercise limitation and goes on to say that, if this isnt having an effect accordingly the treatment should be intensified using eith er a long bronchodilator or a combined therapy with a short acting beta2-agonist and a short-acting anticholinergicThe respiratory system is the major part for squanderes exchange to take place, it renders takes the air that enters are bodies when we inhale and travels through the respiratory system, exchanging atomic number 8 for coke dioxide and expels carbon dioxide when we ex hale (munden, J, 2007). In the NHS there is a tool to sum up 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 long time.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 split of her life.Patients with COPD have traditionally been divided into knock puffers and sullen 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- castingd, 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 impression is widely taught and acknowledged academically, in clinical practice patients tend not to be clearly in one or the other of these 2 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 pa tients may be showing signs of saddle 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 range 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 ruinous 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 mucous secretion layer, and an airway surface liquid (ASL) layer, which work in concert to move back inhaled particles from the lung.The nose and nasal cavity are composed of ciliated columnar epithelium cells which contain chalice cells and cilia, the chalice cells are responsible for secreting mucous secretion which is able to trap the at pathwayiver particles from inspired air and the cilia which are fine hairs that can trap larger particles. The cilia carrys the particles by a sweeping bowel movement 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 go into the lungs (Munden, J, 2007).The twain major sources of mucous secretion 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 c alibre. In chronic respiratory diseases, such as COPD and asthma, submucosal glands increase in coat (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, 1994Jackson, 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 rabble-rousing parameters have been shown to correlate with a reduction in lung function (FEV1) and an magnify bronchoconstriction airway hyperreactivity (AHR) to nonspec ific 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 groovy (Rubin, 2002). This is characterised by the smokers 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(prenominal) form of secreting cell these are important they form ciliated cells and to armed service regenerate the bronchiolar epithelium, they produce hypophase component and a protease inhibitor these attend 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, 1994Jackson, 2001Chronic obstructive pulmonary disease, NICE Clinical Guideline (2004) Management of chronic obstructive pulmonary disease in adults in primary and secondary takeCOPD. BMJ Clinical Evidence. www.clinicalevidence.com, accessed 10 June 2009Textbook of aesculapian 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 Mar97 Suppl CS71-9. abstractChronic obstructive pulmonary disease, NICE Clinical Guideline (2004) Management of chronic obstructive pulmonary disease in adults in primary and secondary careLacasse Y, Goldstein R, Lasserson TJ, et al Pulmonary rehabilitation for chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2006 Oct 18(4)CD003793. abstractBarr RG, Bourbeau J, Camargo CA, et al Inhaled tiotropium for stable chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2005 Apr 18(2)CD002876