Pathophysiology of Emphysema

Emphysema is a progressive ailment of the lungs that occurs due to the inflation of the alveoli. Typically, emphysema is characterized by destruction of alveolar wall and permanent enlargement of airspace of the terminal bronchioles (Manwar, Awandkar, & Khode, 2015). In most case, the term emphysema is used reciprocally with chronic obstructive pulmonary disease (COPD). Despite, the advancement in the field of medicine in Australia, emphysema is still the primary chronic disease, and it has a high prevalence (Jones, Pisano, Elsobky, & Watson, 2015). Recent studies have shown that 60% of the Australians suffer from COPD and it has contributed to thousands of deaths. Moreover, emphysema was more prevalence in men because of their smoking habits, but that is not the case in our contemporary society as women are more vulnerable to the development of emphysema. Typically, COPD is often incurable but mostly preventable and manageable.

The paper seeks to discuss the pathophysiology, and types of emphysema. Understanding the pathophysiology of a condition is essential as it will assist a clinician to manage the disease effectively. Also, the paper will discuss the mechanism of alteration in air compliance, risk factors, diagnostic tests, and the management of both acute and chronic emphysema. Lastly, it will explore on the preventive measures and palliative care of emphysema.

The main function of the lungs is to help in the process of breathing. Respiration is the process whereby the oxygen from the air enters into the red blood cells while the carbon dioxide gas leaves the blood through the process metabolism (Manwar, Awandkar, & Khode, 2015). Lobes are divided parts of the lungs; the left lung has two lobes the lower and upper while the right lungs are made up of three lobes. Usually, when the lung is damaged the process of respiration gets hindered thus, making it difficult for a person to breath well.            

Lung injury is as a result of a vast pathogenic process that takes place within the lungs. Typically, the lung injury might occur because of the destruction or through inflammatory processes when the lungs get exposure to smoke. Usually, when dust or tobacco are inhaled into the lungs, it first comes into contact with the alveoli which prompts the inflammatory response. (Eltboli, 2015). The immune cells include CD8 positive, eosinophils, macrophages, CD4 positive and lymphocytes polymorphonuclear cells. Then the immune cell transports the foreign particles to the bronchial where neutrophilic chemotactic factors are released. Also, macrophages which are high in the alveolar release Proteolytic enzymes which in turn leads to the destruction of the epithelial cell barrier. It is presumed that the release of cytokines reduces the flexibility of the alveolar walls which ultimately leads to the rapture of the alveolar walls (Troy, & Corte, 2015). The late stage of emphysema is associated with fatigue, depression, Wight lose and headache.

Types of Emphysema

 

 Figure 1: Anatomical difference Between damaged and normal alveoli

     

Figure 2: Lung and alveoli

There are two primary types of emphysema centriacinar and panacinar. Centriacinar emphysema is also known as centrilobular. It is the typical pulmonary emphysema mainly found in the upper lobe of the lung and primarily confined to the proximal bronchioles with focal damage. Recent studies have shown that centrilobular is most common among the smokers. According to Schellack, & Omoding, (2015) Smokers are more susceptible to centriacinar because the tobacco smoke infuriates the alveolar macrophages, which in turn triggers the release of neutrophil chemotactic. Typically, the released chemicals are responsible for the damaged of epithelial cell barrier. Also, prolonged smoking which might cause chronic bronchitis, prejudices the smoker to repeated and secondary infections.

On the other hand, panacinar is prime in the lower lobe of the lungs. It is also known as panlobular. Typically, panacinar damage the entire alveolus consistently and it is common among patients with alpha1 antitrypsin (AAT) deficit. Moreover, panacinar is characterized by the permanent destruction of the whole acinus distal. According to Ostridge et al., (2016) Panacinar emphysema is a hereditary condition.   

There are many risk factors associated with emphysema. Typically, the most critical risk factor is tobacco smoking. Recent studies have shown that long-term smoking is the main risk factors that predispose a person to the development of emphysema (Cho et al., 2015). It must be noted that the longer you smoke, the higher the risk of developing the chronic obstructive pulmonary disease (COPD). Usually, the inhaled smoke directly affects the cells which are responsible for clearing the mucus, and it damages lung tissues which result in difficulty in breathing.

Moreover, the second risk factor for emphysema is industrial exposure to chemicals and dust. Recent studies have demonstrated that long-term exposure to vapor, dust, and fumes in a workplace inflame and irritates the lungs which lead to the destruction of epithelial cell barrier. Thirdly, genetics is the risk fact that predisposes a person to the development of emphysema. For instance, genetic disorder alpha1 antitrypsin (AAT) deficit is the primary cause of panacinar emphysema (Oikonomou et al., 2015). The primary function of alpha1 antitrypsin (AAT) is to protect the lungs. Therefore, its deficiency affects the lungs. Recent studies have demonstrated that genetic factors make cigarette smoker more vulnerable to the development of chronic obstructive pulmonary disease (COPD).

Furthermore, individuals with asthma and they smoke are at a higher risk of developing emphysema because the amalgamation of asthma which is an inflammatory respiratory disease, and smoking makes one susceptible to chronic obstructive pulmonary disease. Also, age is another risk factor for emphysema. Typically, COPD develops slowly over a long period, for instance, signs and symptoms of emphysema begin to manifest when one is 40 years old. emphysema is common among old adults. It is a progressive ailment that takes time to develop (Cheng, & Mohammed, 2015,). Lastly, people who are from developing countries are at a higher risk because of smoke from burning fuel. The inhaled fumes from burning fuel irritates the lungs which leads to the destruction of epithelial cell barrier. When the alveoli are damaged an individual will have difficulty in breathing.      

Risk factors of Emphysema	Pathophysiology
Smoking	Emphysema is caused by long-term smoking. Typically, when the smoke is inhaled into the lungs, it first comes into contact with the alveoli which prompts the inflammatory response.
Genetics.	Genetic disorder alpha1 antitrypsin (AAT) deficit is the primary cause of panacinar emphysema. The primary function of alpha1 antitrypsin (AAT) is to protect the lungs. Therefore, its deficiency affects the lungs.
Asthma	Asthma is an inflammatory respiratory disease that makes an individual susceptible to chronic obstructive pulmonary disease.
Age	Typically, emphysema is common among old adults. It is a progressive ailment that takes time to develop. Recent studies have shown that signs and symptoms of emphysema begin to manifest when one is 40 years old.
Industrial exposure to chemicals and dust	long-term exposure to vapor, dust, and fumes in a workplace inflame and irritates the lungs which lead to the destruction of epithelial cell barrier.

Risk Factors for Emphysema

 Table 1: Summary of Risk factors and the pathophysiology of Emphysema.

Lungs compliance refers to the ability of the lungs to expand and stretch. There are two types of compliance static and dynamic. Static compliance is the alteration of the lung volume while dynamic compliance is the alteration of the lungs during air movement (Cooksley et al., 2015). Emphysema is associated with an increase in pulmonary change due to the loss of elasticity and alveolar tissue.

On the other hand, low compliance means a stiff lunge. Thus, there is a need to bring in a standard capacity of air. Typically, low compliance is associated with lung fibrotic, where the lungs loss its distensibility and become harder. According to Scott et al., (2014) high compliance is as a result of the damaged elastic tissue by the enzymes released in response to the inhaled irritants, such as dust, tobacco smoke, and fumes from burning fuel. Therefore, it will lead to an increase in airway compliance because of poor elastic recoil. Patients with emphysema have enormous difficulty in both exhaling and inhaling air.

The diagnostic test of emphysema is a process that involves a series of examination as the ailment cannot be substantiated with only one analysis. Also, a clinician cannot go with symptoms alone as some symptoms are related to other respiratory conditions (Wright, 2018). Checking on the family history is an essential step as it will establish if there is any genetic link related to the disease. Also, pulmonary function testing (PFT) is a crucial test as it helps a clinician to make a definite diagnosis. PFT test involves a series of breathing examination that measures the volume of air and airflow in the lungs. Pulmonary function test is critical as it enables a clinician to assess the function of the lungs.

Moreover, the chest x-ray is essential as it will enable a physician to confirm the diagnosis of emphysema and rule out other lung conditions. However, the physician cannot diagnose emphysema with x-ray alone. The use of CT scan will give a clear picture of the damaged alveoli. Additionally, physical examination cannot be ruled out as it assists a clinician to identify unusual activity (Reddel, 2015). For instance, physical examination helps to determine if the patient is having difficulty in breathing out. Lastly, arterial blood gases analysis measure how well the lungs distribute oxygen to the blood and remove carbon dioxide. If the red blood cells have low oxygen that’s an indication of emphysema. It is undeniable that all Diagnostic test of emphysema is critical as one test cannot be overlooked over the other.

Alteration in Airway Compliance and Lung Compliance

Despite, the effort of the Australian government to educate the public on the dangers of smoking, chronic emphysema is still the major health problem, and it is the leading cause of death. Emphysema is a serious condition because it hinders adequate supply of oxygen to the vital organs of the body. Moreover, emphysema is often incurable but mostly preventable and manageable. There are various treatment options for emphysema. The first treatment is bronchodilators medication which improves airflow by relaxing the bronchiolar muscles. It can be used either for short-term use or a prolonged period (McElvaney et al., 2017). Also, oral treatment is essential as antibiotics help to prevent server infection like pneumonia.

Additionally, oxygen supplementation is essential as people with emphysema often need to use oxygen treatment because they have difficulty in breathing. Lastly, rehabilitation and surgery are a vital treatment as it helps to reduce lung volume thus, decrease in symptoms. Also, breathing exercises are a significant rehabilitation process that helps to strengthen the lungs. Table 2 summarizes the primary medication that is used to treat emphysema.

Medication	Mechanism of Action	Dose	Duration	Side effect and interactions
Bronchodilators e.g. Albuterol (Vospire ER	Bronchodilators are medications that makes breathing easier by opening the airway. It is taken using a nebulizer or inhaler.	2 puffs 180mcg	4 to 6 hours	Bluer vision, cough, tremors and dry mouth. The medication affects individuals with heart conditions.
Corticosteroids e.g. Prednisolone	Corticosteroid help to reduce tenderness in the body which will assist air flow in the lungs. Fluticasone are either taken through injection or by mouth	5 mg/day to 60 mg/day for adults and for children 0.14 to 2 mg/kg/day PO	24 to 48 hours	Wight gain, upset stomach upset, and Muscles weakness. It decreases the immune system as it reduces symptoms such as swelling.
Methylxanthines e.g. Theophylline	The drug relaxes the muscles and it act as an anti-inflammatory drug. It comes as a liquid or a pill that an individual takes daily. It is used when the Corticosteroid and Bronchodilators don’t work.	0.3 mg/kg/hour IV to 800mg/day for adults and 0.4mg/kg/hour to 900mg/day	6 to 8 hours	Tremor, trouble sleeping, headache and vomiting or nausea.
Roflumilast	Roflumilast helps to relieve tenderness which will improve air flow in your lungs. It comes as a pill and it is taken one per day.	250 mcg po	4 weeks	Tremors, stomach upset, Wight loss and cramps. Its severe reaction includes depression and suicide thoughts.

Palliative care is essential in managing both acute and chronic emphysema. Its goal is to help patients receive the best quality of life by dismissing crushingly emotional and physical symptoms (Fingleton et al., 2017). Also, palliative care help patient to change on their lifestyle habits like smoking. Lastly, palliative care assists in effective disease management and medication.

The most practical way to prevent emphysema is to avoid smoking. Also living a healthy lifestyle will help to reduce the chance of developing emphysema. For instance, regular exercise and eating strengthen the lungs muscles thus, improving airflow (Silva, Oyarzún, & Olloquequi, 2015). Also, individuals who work in the chemical industry should wear the protective mask to protect the lungs from exposure to harmful fumes.

Conclusion

Emphysema is a progressive ailment of the lungs that occurs due to the inflation of the alveoli. Despite, the advancement in the field of medicine in Australia, emphysema is still the primary chronic disease, and it has a high prevalence. Recent studies have shown that 60% of the Australians suffer from COPD and it has contributed approximately to thousands of deaths. There are two primary types of emphysema centriacinar and panacinar. Typically, the most critical risk factor is tobacco smoking. The effective way to prevent emphysema is to avoid smoking tobacco.

References

Cheng, S., & Mohammed, T. L. H. (2015, January). Diffuse smoking-related lung disease: emphysema and interstitial lung disease. In Seminars in roentgenology (Vol. 50, No. 1, pp. 16-22). Elsevier.

Diagnostic Tests for Emphysema

Cho, M. H., Castaldi, P. J., Hersh, C. P., Hobbs, B. D., Barr, R. G., Tal-Singer, R., … & Coxson, H. O. (2015). A genome-wide association study of emphysema and airway quantitative imaging phenotypes. American journal of respiratory and critical care medicine, 192(5), 559-569.

Cooksley, N. A., Atkinson, D., Marks, G. B., Toelle, B. G., Reeve, D., Johns, D. P., … & Walters, E. H. (2015). Prevalence of airflow obstruction and reduced forced vital capacity in an A boriginal A ustralian population: The cross?sectional BOLD study. Respirology, 20(5), 766-774.

Eltboli, O. M. (2015). Eosinophilic airways inflammation in Chronic Obstructive Pulmonary Disease (Doctoral dissertation, Department of Infection, Immunity and Inflammation).

Fingleton, J., Travers, J., Williams, M., Charles, T., Bowles, D., Strik, R., … & Dooney, N. (2015). Treatment responsiveness of phenotypes of symptomatic airways obstruction in adults. Journal of Allergy and Clinical Immunology, 136(3), 601-609.

Jones, A., Pisano, U., Elsobky, S., & Watson, A. J. (2015). Grossly delayed massive subcutaneous emphysema following laparoscopic left hemicolectomy: A case report. International journal of surgery case reports, 6, 277-279.

Manwar, S. J., Awandkar, S. P., & Khode, N. V. (2015). Subcutaneous emphysema (Windpuff) in a Giriraj poultry. Veterinary Practitioner, 16(2).

McElvaney, N. G., Burdon, J., Holmes, M., Glanville, A., Wark, P. A., Thompson, P. J., … & Seersholm, N. (2017). Long-term efficacy and safety of α1 proteinase inhibitor treatment for emphysema caused by severe α1 antitrypsin deficiency: an open-label extension trial (RAPID-OLE). The Lancet Respiratory Medicine, 5(1), 51-60.

Oikonomou, A., Mintzopoulou, P., Tzouvelekis, A., Zezos, P., Zacharis, G., Koutsopoulos, A., … & Prassopoulos, P. (2015). Pulmonary fibrosis and emphysema: Are the emphysema type associated with the pattern of fibrosis? World journal of radiology, 7(9), 294.

Ostridge, K., Williams, N., Kim, V., Harden, S., Bourne, S., Coombs, N. A., … & Wilkinson, T. M. (2016). Distinct emphysema subtypes defined by quantitative CT analysis are associated with specific pulmonary matrix metalloproteinases. Respiratory research, 17(1), 92.

Reddel, H. K. (2015). Treatment of overlapping asthma–chronic obstructive pulmonary disease: Can guidelines contribute in an evidence-free zone? Journal of Allergy and Clinical Immunology, 136(3), 546-552.

Schellack, N., & Omoding, R. (2015). Chronic obstructive pulmonary disease: an update. SA Pharmaceutical Journal, 82(6), 24-29.

Scott, D., Burke, K., Williams, S., Happell, B., Canoy, D., & Ronan, K. (2014). Increased prevalence of chronic physical health disorders in Australians with diagnosed mental illness. Australian and New Zealand Journal of Public Health, 36(5), 483-486.

Silva, R., Oyarzún, M., & Olloquequi, J. (2015). Pathogenic mechanisms in chronic obstructive pulmonary disease due to biomass smoke exposure. Archivos de Bronconeumología (English Edition), 51(6), 285-292.

Troy, L., & Corte, T. (2015). Interstitial lung disease in 2015: where are we now? Australian family physician, 44(8), 546.

Wright, A. (2018). Survey of Aboriginal smokers’ and ex?smokers’ knowledge, attitudes and behaviours in Central Australia 2016–2017. Australian Journal of Rural Health, 26(4), 251-257.