PATHOPHYSIOLOGICAL PROCESS TEMPLATE

Transcription

1 1 PATHOPHYSIOLOGICAL PROCESS TEMPLATE DISEASE: Chronic obstructive pulmonary disease (COPD) DEFINITION: COPD can be defined as a disease in which there is a significant damage to the lungs thus reducing the lung capacity and constriction of air ways making breathing very difficult and exhaustive for patient. There are two major form of disease namely emphysema and chronic bronchitis AETIOLOGY: Active smoking for a long period of time with high number of cigarettes per day is the basic etiology behind acute exacerbation of disease. There are other factors as well like age of patient, her immunity etc but primary reason is her past history of smoking. PATHOGENESIS In COPD there is a formation of various anatomical lesions like losing of lung elastic recoil capacity; there is fibrosis of the tissue in lungs and constriction of air ways due to increased production of sputum as a result of infection and allergic reactions. Smoking basically lead to release of oxidants and protease in lungs which initiates inflammatory reactions and them also hinder the lung repairing capacity thus causing damage to lung walls and linings of alveoli (Kumar and Clark, 2005). Tobacco smoke has excessive quantities of free radicals which creates a stress on the lungs. This stress is known as oxidative stress and it enables the lining and other organic parts of the lungs to get oxidized. Cytokine is the chemical which is released by the

2 2 body as a inflammatory process when a irritant like smoke affects the lungs leading to inflammatory responses and damages to the lung tissues. CLINICAL FEATURES Breathlessness, difficulty in taking stairs, early exhaustion in routine work, increased production of sputum, continuous coughing, reduced lung capacity, lowered intake of air volume, dysapnea and ronchi etc. COURSE OF DISEASE In case of acute exacerbations it is observed that sudden infection or environmental pollutant triggers the exacerbation and it lasts for a few days with proper medical care and management. Management includes antibiotics regime along with broncho dilators, anti asthmatics and anti inflammatory drugs. In case of misdiagnosis or non compliance from patient situation can worsen leading to permanent lung damage, lung cancer or fatality (Kelsen, 2007).

3 3 COMPLICATIONS: Respiratory failure, sever constriction of air way leading to breath arrest, continued smoking leading to lung rupture, bleeding, necrosis, carcinoma etc (Loscalzo, et al. 2008). PROGNOSIS: If patient leaves smoking habits, causative reasons and take proper medications then prognosis is good and in a period of 7-15 days of treatment patient can resume the normal routine but in case of noncompliance prognosis is very poor and it can lead to severe respiratory complications and eventual death of patient. DIAGNOSIS: Acute Exacerbation of COPD TREATMENT: Oxygen 2l/min through nasal pongs Salbutamol 400 Ug and ipratropium 80 Ug through inhaler /4hrs Prednisolone 40 mg/ od x 7 days Doxycycline 100 mg /od x 7 day (Ram, 2011).

4 4 PREVENTION Avoiding environmental pollutant, passive or active smoking of any kind, stress and regular exercising, keeping weight under control and taking care in winter and rainy season are some of the measures which can prevent further episodes like this. TASK 2 Q.1 Explain the pathogenesis that leads to the structural and functional changes resulting from Mrs White s chronic obstructive pulmonary disease? Ans:- change in air way size and constriction of bronchial passage is a direct response of inflammatory action of irritants like smoke, pollutant etc in the lungs and this lead to a structural change. There are three major changes in the anatomy of lungs which creates the problem of restrictive breathing namely:- peribronchial fibrosis, development of scar tissues and excessive formation of epithelial cells in response to the inflammation and damages. Alveoli linings get destroyed and they are the building blocks of lungs thus reducing the breathing and air intake capacity of lungs. Parenchymal destruction is also seen which is in association with loss of the elastic capacity of lungs. If lungs losses their elastic capacity then they won t be able to deflate and inflate in breathing process creating shortness of breathes. Along with other chemicals cigarette smoking also lead to formation of tar inside the lungs which gets collected in the lungs at the bottom. It also impacts the lung capacity and damages the structural integrity of lungs (Rennard and Vestbo, 2006).

5 5 Over the period of time necrosis, destruction of alveoli and linings, inflammatory response because of smoke creates an ideal spot for opportunistic bacteria to attack and infect the region leading to acute exacerbation and sudden collapse of patient. It is also observed that in case of patient with advanced COPD have primary chronic bronchitis rather than emphysema and it is also known as blue bloaters where patient have blue skin color, cornea color and lip color. All these symptoms were present in Mrs. White when she was brought to the hospital making it clear that she is suffering from acute exacerbation of COPD in an advanced stage (Halbert, 2006). Q.2 Explain how three of Mrs White s clinical manifestations are related to the structural and functional changes of her chronic obstructive pulmonary disease? Ans:- Three clinical manifestations which are observed in Mrs. White when she was brought to the hospitals were centrally cyanosed condition, pursued lips and severe dyspoenia. All these clinical manifestation of the structural and functional changes in the lungs and breathing capacity is because of acute exacerbation of COPD. Lungs are the organ where blood and inhaled air are exposed to each other through alveoli. At this juncture carbon di oxide from blood is diffused in air while oxygen is absorbed from the air. Higher the surface area of alveoli better exchange of gases and diffusion in blood take place. When structural and functional integrity of lungs get compromised because of disease like COPD there is a immediate reduction in exchange of gases activity and blood remains deoxygenated when it is circulated back to the body. This leads to condition like central cyanosis. Similarly severe dyspnea is showing that body is struggling to take proper breaths and oxygenate the blood and because of

6 6 lung s reduced capacity it is not able to causing shortness of breath. Pursed lips are a sign of extra effort done by involuntary muscles of the body to inhale as much air as possible (Longmore, et al. 2004). Q.3 Select two drugs that have been used to treat Mrs White s chronic obstructive pulmonary disease. Discuss the rationales for the administration of these drugs. Relate your discussion to the pathophysiological process. Ans:- two drugs which is used for the management of Mrs. White s COPD are salbutamol 400 mg and prednisolone 40 mg orally. Rationales of administrating these two drugs are as follows Salbutamol is a beta 2 agonist which acts as a bronchodilator because it relaxes the smooth muscles of bronchia leading to expanded airway for breathing. Salbutamol act on the beta 2 adrenergic receptors present on the smooth muscles of bronchia and relaxes the muscles. It is a very fast action short acting beta two agonist which is primarily used for immediate relief in COPD (Kumar, 2009). Prednisolone is a corticosteroid which is a anti inflammatory and anti histamine drug. It prevents acute exacerbation of COPD in future and also reduces the impact of inflammatory irritants in airway thus reducing the excessive production of sputum etc. corticosteroids also assist in healing process of the damaged lung tissue and they reduces the swelling and inflammatory responses of alveoli lining which is forms the structure of lungs. Both drugs help in restoration of the structure and functionality of the lungs which is damaged by COPD.

7 7 REFRENCES BOOKS Kumar, P. and Clark, M (2005) Clinical Medicine (6th ed.). Elsevier Saunders. pp ISBN Longmore, M. et al. (2004) Oxford handbook of clinical medicine, Oxford [Oxfordshire]: Oxford University Press. pp ISBN Ram, FS (2011) "Tiotropium mist inhaler for COPD increases risk of mortality compared with placebo". Evidence-based medicine 16 (6): doi: /ebm PMID Loscalzo, J. et al. (2008) Harrison's Principles of Internal Medicine (17th ed.). McGraw-Hill Professional. ISBN Kumar, V. (2009) Robbins Pathologic Basis of Disease. p JOURNALS Halbert, J. (2006) "Global burden of COPD: systematic review and meta-analysis". Eur. Respir. J. 28 (3): doi: / PMID Rennard, S. I.; Vestbo, J. R. (2006) "COPD: the dangerous underestimate of 15%". The Lancet 367 (9518): doi: /s (06)

8 8 Kelsen, S et al. (2007) "The safety and efficacy of infliximab in moderate to severe chronic obstructive pulmonary disease". Am. J. Respir. Crit. Care Med. 175 (9): doi: /rccm oc. PMID