Tuesday, November 26, 2019
Chronic Obstructive Lung Diseases (Copd) Essays
Chronic Obstructive Lung Diseases (Copd) Essays Chronic Obstructive Lung Diseases (Copd) Paper Chronic Obstructive Lung Diseases (Copd) Paper Chronic Obstructive Lung Diseases (Copd) Introduction: In this paper I am going to discuss Chronic Obstructive lung Diseases (COPDs) which is caused due to partial or complete obstruction by an increase in the resistance to air flow. Excluding tumor and foreign body, the obstructive disorders include: 1. Asthma 2. Emphysema 3. Chronic bronchitis 4. Bronchiectasis 5. Cystic fibrosis 6. Bronchiolitis However Emphysema and chronic bronchitis are the major obstructive pulmonary disorders. In all these diseases, the hall mark is a decreased expiratory flow rate (FEV1: FVC ratio) with either increased or normal total lung capacity. Methodology: In order to complete this paper I searched the internet for various sources, did extensive reading and compared various obstructive pulmonary diseases. Result: In Emphysema destruction of the terminal bronchioles occur leading to abnormal enlargement of air spaces. TYPES: It is classified according to the anatomic distribution of the lesion with in the acinus. a.      Centriacinar: involves upper lobes of lung and apices, usually seen in male smokers along with chronic bronchitis. Bullae may rupture and lead to spontaneous pneumothorax. b.  Panacinar: Predominant in anterior margins of the lungs. It causes uniform destruction and enlargement of the air spaces. It is strongly associated with a-1 antitrypsin deficiency. c.  Paraseptal: involves distal acinus and pleura, in areas of fibrosis and scars. It may lead to spontaneous pneumothorax. d.  Irregular: occurs in cases of old scarred lung from TB, histoplasmosis etc.usually remains  symptom less[1]. Enphysema can be also be classified as 1.  COMPENSATORY EMPHYSEMA: it is a condition in which hyper inflated lungs are found as result of compensation, mostly due to loss of lung substance during unilateral pneumonectomy. 2.  SENIL E EMPHYSEMA: In this type lungs are expanded due to age. It is mostly asymptomatic with no destruction of walls. 3.   OBSTRUCTIVE INFLATION: This condition is due to a tumor or foreign body causing sub total obstruction resulting in lung expansion because of trapped air in the alveolar spaces. Emphysema is aggravated by smoking because smoke particles activate macrophages which in turn recruit neutrophils from the circulation, elastase an enzymes is released from neutrophils which further enhances macrophage elastase activity. An important role is played by free radicals released from activated neutrophils which inactivates a-1 antitrypsin by releasing oxidants. Morphology shows boggy and voluminous lungs. Microscopically air spaces are enlarged, rupture of their thin walls show Honey combing appearance. Capillaries are compressed and contain no blood. Chronic Bronchitis: Described as persistent cough with sputum for atleast 2 consecutive years for atleast 3months.The cause is usually chronic irritation of airways by the substances inhaled esp tobacoo smoke. Smoke illicit bronchitis by eliciting excess mucus secretion with hypertrophy of mucus glands, brochioloitis and metaplasia of bronchiolar epithelium. The injury initiated by smoke is further aggravated by secondary infections[2]. It usually occur in these forms: 1.  Simple chronic bronchitis: It is characterized by marked sputum production, mucoid in nature.The airflow is not obstructed . 2.  Chronic mucopurulent bronchitis: It is mostly after secondary infection followed by simple bronchitis. Sputum contains pus. 3.   Chronic asthmatic Bronchitis: Individuals with hypersensitive airways showing intermittent episodes of asthma and demonstrating chronic bronchitis. Morphology shows a.congestion and edema of mucous membranes of lung, b.hypertrophy of mucus glands, c.filling of air spaces by mucinous secretion, d.mucus plugs, imflamation and fibrosis in bronchioles, e. change of bronchiolar epithelium from columnar to squamous epithelium f. decreased number of cilia Clinical Features Of Copds: Early stage of disease are asymptomatic because of pulmonary reserve function, later on, with the progression of disease, a wide variety of symptoms are observed. The spectrum of disease are designated in two extremes, type A and type B. Mostly , features of both type A and type B are present in a single case[3]. Type A patients:            Present with chronic cough either dry or prductive of mucoid f sputum ; progressive dyspnea, and wheezing. They hyperventilate and often sit hunched forward (to bring accessory respirator muscles into action) with mouth open and nostrils dilated in an attempt to overcome the ventilatory difficulty. Their lungs are over inflated with increase anteroposterior diameter of the chest (â€Å"barrel chest†) and flattened diaphragm on chest xray. These patients successfully maintain oxygenation of the blood by hyperventilation. Patients with type A COPD are sometimes called â€Å"pink puffers†. Type B patients: Have marked chronic obstructive bronchitis and canno hyperventilate. There is decreased oxygenation of blood (cyanosis) and increased arterial carbon dioxide content. They also have pulmonary hypertension caused by changes in themicrovasculature of the lung parenchyma. This leads to right ventricular hypertrophy and failure (â€Å"cor pulmonale†), and peripheral edema due to right heart failure is a dominant clinical feature . Type B patients are sometimes called â€Å"blue bloaters†The correlation between these clinical types and pathologic changes is inexact. Type A patients frequently have dominant emphysematous changes while type B patients usually have dominant chronic obstructive bronchitis. Most patients however have varying mixtures of both pathological changes and clinical features. In type B patients with chronic hpercapnia (elevated) Pco2) , the respirator centre becomes insensitive to the Pco2 stimulus and is driven by the hypoxemia. Administration of oxygen in these patients can remove the respiratory centre drive and cause carbon dioxide retention and death (â€Å"carbon dioxide narcosis†)[4]. Pathogenesis The protease antiprotease hypothesis holds that destruction of alveolar walls in emphysema stems form and imbalance between proteases and their inhibitors in the lung. The evidence is as follows:  ·Ã‚        Individuals with a hereditary deficiency of the major protease inhibitor, alpha-I-antitrypsin, invariably develop emphysema, and at a younger age if they smoke.  ·Ã‚        Pulmonary instillation of proteolytic enzymes, including neutrphil elastase, results in emphysema in experimental animals. EMPHYSEMA AND CHRONIC BRONCHITIS Predominant bronchitis Predominant Emphysema Age (yr) 40-45 50-75 Dyspnea Mild, late Severe, early Cough Early, copious sputum Late, scanty sputum Infections Common Occasional Respiratory insufficiencies Repeated Terminal Cor pulmonale Common Rare, terminal Airway resistance Increased Normal or slightly increased Elastic recoil Normal Low Chest radiograph Prominent vessels; large heart Hyperinflation, small heart Appearance Blue bloater Pink Puffer Conclusion:  COPD covers a broad spectrum of pulmonary diseases. One of the most important and preventable leading factor for COPDs is smoking. One should avoid smoking. Work Cited Page: 1.     Quinn, Campion E. 100 Questions Answers About COPD. Jones and Bartlett Publishers, Inc, 2005. 2.     Currie, Graeme P. ABC of COPD. BMJ Books, 2006. 3.     Schneider, Arthur S., Szanta Philip A.Pathology.Lippincott Willians Wilkins. 4.     Cotran, Ramzi S., Vinay Kumar, Tucker Collins. Pathologic Basis of Disease.W.B. Saunders Company. [1] Quinn, Campion E. 100 Questions Answers About COPD. Jones and Bartlett Publishers, Inc, 2005, pp 65-89. [2] Currie, Graeme P. ABC of COPD. BMJ Books, 2006.pp10-35. [3]Schneider,Arthur S., Szanta Philip A.Pathology.Lippincott Willians Wilkins,pp 70-135. [4] Cotran , Ramzi S., Vinay Kumar, Tucker Collins.Pathologic Basis of Disease.W.B. Saunders Company ,pp 134-190.
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