logo

Pathophysiology of COPD2 chronic obstructive pulmonary disease

   

Added on  2021-06-18

16 Pages3343 Words92 Views
Materials Science and EngineeringDisease and DisordersHealthcare and Research
 | 
 | 
 | 
Running head: chronic obstructive pulmonary disease 1Chronic obstructive pulmonary diseaseName:Institutional affiliation:
Pathophysiology of COPD2 chronic obstructive pulmonary disease_1

COPD 21.1Pathophysiology of COPDChronic Obstructive Pulmonary disease (COPD) is a form of obstructive lung disease where there is a change in the normal structure of central airways, peripheral bronchioles and lung parenchyma. Among other factors such as genetics, air pollution and occupational factors, itprimarily results from cigarette smoking which acts as the noxious stimuli. It produces an inflammatory response involving neutrophils, granulocytes, macrophages and to some extent T Lymphocytes (CD8+). These immune cells (polymorphonuclear leukocyte and macrophage) release elastases which cause lung destruction, elastases are insufficiently inhibited by protease inhibitors (Mitchell, 2015).Elastases (Human leukocyte elastase) and an increase in oxidative stress caused by free radicals of Cigarette are usually the primary offender that usually cause the cascade of events that lead about lung destruction, narrowing and inflammation of the airways. This results in an inability to breathe out fully and increased total volume of air in lungs (hyperinflation) which causes shortness of breath. It is usually accompanied by airway hyperresponsiveness to irritants. There is usually a worsening of symptoms during exacerbations as there is a worsened gas transfer and increased inflammation.The overall effect is usually a decreased oxygen levels in blood with an increased concentration of carbon(IV)oxide caused by improper ventilation. The decreased O2 levels after some time causes narrowing of arteries in lungs and breakdown of capillaries thus leading to increased blood pressure in pulmonary arteries (Kawut & Poor,2014).
Pathophysiology of COPD2 chronic obstructive pulmonary disease_2

COPD 3Disease processes contained in COPDChronic bronchitis is usually associated with production of large amounts of sputum as a result of mucous gland hyperplasia which is its histologic hallmark. There are usually structural changes which include ciliary abnormalities, atrophy, metaplasia and bronchial wall thickening. Inflammation and secretions accompanied with it causes obstruction. These changes and an additive effect of loss of alveolar attachment results in limitation of ventilation.Emphysema is an irreversible enlargement of air spaces distal to terminal bronchioles, this causes a decrease in surface area for gaseous exchange. There is also a decrease in elastic recoil and airway narrowing as a result of loss of alveolar supporting structures. Inability to oxygenate properly is as a result of destruction of alveolar septae. A V/Q mismatch is also experienced as there is limited perfusion in a well-ventilated lung. The overall resultant effect is usually muscle wasting and weight loss (Sohal, 2016).1.2Acute Exacerbation of COPDThis is usually some sudden worsening of COPD symptoms characterized by a significant increase in both shortness of breath and intensity of coughing. It is typically caused by an infection by either bacteria or virus, in most cases this lasts for several days. The infection causes a change in sputum appearance to green yellow. In some cases, it might also be caused bytoxins especially environmental pollutants. Symptoms of exacerbation include increased coughing, significant chest congestion, shortness of breath that is associated with wheezing. Thissudden worsening of COPD symptoms might cause rupturing of the airways hence leading to pneumothorax (Zhou & Li, 2015).
Pathophysiology of COPD2 chronic obstructive pulmonary disease_3

COPD 4In Robert’s case, he developed an exacerbation due to infection by a community acquiredpneumonia, the exacerbation lasted for about 3days. He was put under non-invasive ventilation to aid in breathing as it is usually associated with significant decrease in ability to ventilate properly. He was at a high risk of developing exacerbation or rather having the COPD itself since he has been smoking for the past 40 years or might have refused to follow a drug therapy after being diagnosed of COPD, this include improper use of inhalers or failure to take the prescribed drugs. The infection then worsened the situation making hence developing an exacerbation. Other factors that may cause this include exposure to certain allergens (such as wood, pollen) and air pollution.To some extent, exacerbations can be prevented by smoking cessation, immunization to certain pathogens such as pneumococcal vaccinations, maintain a good diet and avoiding contact with people already infected with certain pathogens. In Robert’s case, he should follow these measures to reduce the chances of this event happening again. He should also follow the right regimen of medication to ensure that there is proper management of the COPD symptoms. Although there is no known cure, these measures will significantly improve his life.
Pathophysiology of COPD2 chronic obstructive pulmonary disease_4

End of preview

Want to access all the pages? Upload your documents or become a member.

Related Documents
Pathophysiology of COPD, Acute Exacerbation, Pneumonia, and Interventions for COPD Management
|10
|2873
|82

Nursing Care and Education for COPD Exacerbation: A Case Study
|13
|2620
|343

Understanding Chronic Obstructive Pulmonary Disease (COPD)
|2
|577
|103

Chronic Obstructive Pulmonary Disease (COPD) | Case Study Analysis.
|13
|3687
|17

(PDF) Pathophysiology of Chronic Obstructive Pulmonary Disease (COPD)
|16
|3650
|128

Best Medical Surgical Nursing Assignment
|10
|2775
|31