A Short Note On Obstructive Pulmonary Disease And Its Acute- Exacerbation

Lungs – Mucus plugging, chronic bacterial infections, pronounced inflammatory response, damaged airways leading to respiratory insufficiency, progressive decline in pulmonary function.

Chronic inflammation leads to structural changes, narrowing of the small airways, and destruction of lung tissue, which diminishes the ability of the airways to remain open during expiration

Nasal polyps can develop but only need to be removed if they become irritating. The most lethal symptom is related to the lungs. With the large amounts of the thick and sticky mucus, infections cause become more common, decreases the ability to fight infections, and causes swelling and inflammation. This restricts the overall function of the lungs leading to emphysema, bronchitis, bronchiolitis, and pneumonia. With infections, mucus production increases making the disease worse and could result in death. A symptom of the excess mucus is coughing in order to remove mucus. It also plugs up the smaller passageways in the lungs, decreasing the lung’s volume. Inadequate air supply results in tiredness, shortness of breath, and intolerance of

Abnormally thick, abundant secretions from mucous glands can lead to a chronic, diffuse, and obstructive pulmonary disorder in almost all patients.

The client’s secondary diagnosis is community-acquired pneumonia. Typically, immune defense mechanisms, such as the secretion of alveolar macrophages and immunoglobulins A and G, protect the lower airway from infection. Streptococcus pneumoniae, the most common causative agent of community-acquired pneumonia, invades the lungs. The organism triggers an inflammatory response, resulting in increased blood flow and vascular permeability. Neutrophil activation occurs, to surround the kill the invading organism. A combination of the offending organism, neutrophils and fluid from the surrounding blood vessels flood the alveoli, inhibiting normal oxygen transportation. This filling of the alveoli may lead to tachypnea, tachycardia and dyspnea. Further obstruction of airflow and an increased impairment of gas exchange occur as mucous production increases. When

When the respiratory tissue damaged, the body’s inflammatory responses cause the lining of the airways to become swollen and thickened as a result of constant irritation that leads to an excessive mucus secretion in effort to protect the lungs from inhaled irritants such as cigarette smoking, air pollution, passive smoking, occupational dusts and chemicals (Currie 2009).

reaction in which the bronchial tubes in the lungs swell and become blocked with mucous. The

As a result of R.S.’s chronic obstructive pulmonary disease (COPD), he’s going to be experiencing the many consequences of his type B COPD, otherwise known as chronic bronchitis. Copstead & Banasik (2013) states that the pathogenesis for chronic bronchitis has changes in the airways that include swelling and chronic inflammation of the bronchial mucosa which can lead to scarring. In addition, there is hypertrophy of mucosal glands and goblet cells, which leads to increased mucosal production. In chronic bronchitis, there’s also a hypersecretion of bronchial mucous (Copstead & Banasik, 2013, p. 483). In normal conditions, the mucus produced by the mucus glands aids in the protection of the lungs by capturing the foreign particles that enter into the lungs. Bellamy & Booker (2004) report that when long-term smokers such as R.S., who are already developing chronic airflow obstruction, the excess of hypersecretion of mucus contributes to the decline of lung function. Long-term production of mucus may cause the patient to suffer lower respiratory tract infection (p. 19).

The clinical findings that correlate with M.K’s Chronic bronchitis are the chronic cough with sputum and the fact that she has smoked for twenty-two years. Chronic bronchitis is defined as a daily cough with sputum production for at least three consecutive months for two years in a row. Chronic bronchitis is also usually associated with long term tobacco use. When you have COPD, the airways of the lungs become inflamed and thickened which make them narrow. They can become clogged with mucus and makes it difficult for air to get in and out of the lungs. Which leads to persistent coughing as your body tries to get rid of the extra mucus.

Patients that do have chronic bronchitis ( B COPD) typically exhibit shortness of breath on exertion, excessive amounts of sputum, chronic cough, and evidence of excess bodily fluids (edema, hypervolemia). Chronic cough tends to be most severe in the mornings, is productive, and occurs for more than 3 months and occurring each year for at least 2 consecutive years. In addition, patients tend to complain about chills, malaise, muscle aches, fatigue, loss of libido, and insomnia. Smoking is also a typical clinical manifestation and is the leading cause of B COPD (accounting for 90% of cases). Late signs include right-sided heart

disease get worse over time. It can cause coughing that produces large amount of mucus,

Following the pathologic changes of chronic bronchitis and bronchiectasis, many patients will present with the following symptoms: shortness of breath, difficulty breathing, wheezing, productive cough and hemoptysis (Stauffer). Many of these symptoms will occur after the patient has recently contracted common cold viruses or other irritants as they weaken the body’s natural balance in the respiratory tract. With the majority of patients having a sudden increase of mucus production, this will have a tendency to obstruct the airways and prevent ventilation. In some cases the patient is able to clear the airway of the obstruction simply by coughing, but excessive coughing can lead to a much more problematic bronchospasm. Also, due to the weakened airway of bronchiectasis patients and increased thick sputum, coughing may prove to be vastly ineffective. These diseases are diagnosed with a combination of examinations such as Pulmonary Functions Tests (PFT), Chest

Approximately half of smokers with chronic bronchitis will stop coughing after one month of smoking cessation. Most patients will no longer cough with continued abstinence from smoking. “People with chronic bronchitis are prone to contracting influenza and Streptococcus pneumoniae infections.” If airflow obstruction has occurred this can improve but the improvement level depends on the duration of injury and the compliance with therapy. Obviously, the more impaired patients will have a lesser recovery of lung function. Conversely, those individuals that have continued bronchial irritation have only a fair to poor prognosis, since repeated fight with the disease usually get worse, with affected individuals having more frequent incidents of coughing and dyspnea over time and further progression of lung function abnormalities. The overall 10 year mortality rate following the diagnose of chronic bronchitis is 50 percent, with respiratory failure following an acute exacerbation being the most frequent terminal event. Such acute exacerbation, are often precipitated by bacterial infection, manifested by purulent sputum, fever and a worsening of the symptoms of poor ventilation. Other known precipitants

Health risks involving the effects of how excess mucus in the lungs causes respiratory problems and how it prevents the pancreas from releasing digestive enzymes that break down food and absorb vital nutrients will be discussed (Cystic Fibrosis Foundation, 2016). An intervention and treatment plan will be tailored to the individual and include specialized management and care of dedicated and specialized medical professionals. Therapies will be discussed and implemented that will provide techniques, equipment, and medicines that will loosen and thin mucus to clear the airways, reduce infections, and improve the absorption of vital

Pulmonary edema is commonly caused by congestive heart failure and fluid overload (Huether & McCance, 2012). With pulmonary edema, there is an increased amount of secretions in the alveoli due to increased hydrostatic pressure in the pulmonary capillaries causing fluid to move in the lung (Tazibr, 2016). There is also an increased amount of secretions in the alveoli due to damaged cilia from smoking. These secretions accumulate and cause further airway obstruction and impair gas exchange. Smoking also deposits nicotine, tar, and oxidant particles in the alveoli (NCBI, 2010). Although the immune response assists with these toxins, prolonged smoking decreases the immune response. For example, a person coughs when he or she smokes that first cigarette. Coughing diminishes over time as a person becomes accustomed to smoking. The rate that macrophages assist with removing toxic particles decrease over time as well (NCBI, 2010) and the efficacy of macrophages decrease with pulmonary edema. The combination of pulmonary edema and chronic over inflation with emphysema greatly impairs the gas exchange at the alveolar