Emphysema anatomy: Emphysema – Physiopedia

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Emphysema – Physiopedia

Pulmonary emphysema, a progressive lung disease, is a form of chronic obstructive pulmonary disease (COPD). Emphysema is primarily a pathological diagnosis that affects the air spaces distal to the terminal bronchiole. It is characterized by abnormal permanent enlargement of lung air spaces with the destruction of their walls without any fibrosis and destruction of lung parenchyma with loss of elasticity.^[1]

There are three types of emphysema; centriacinar, panacinar, paraseptal. See image 1.

Centriacinar emphysema affects the alveoli and airways in the central acinus, destroying the alveoli in the walls of the respiratory bronchioles and alveolar ducts ^[2] .
Panacinar emphysema affects the whole acinus ^[2] .
Paraseptal emphysema is believed to be the basic lesion of pulmonary bullous disease ^[2].

Emphysema, as a part of COPD, is an illness that affects a large number of people worldwide. In 2016, the Global Burden of Disease Study reported a prevalence of 251 million cases of COPD globally. Around 90% of COPD deaths occur in low and middle-income countries .

The prevalence of emphysema:

In United States is approximately 14 million, which includes 14% white male smokers and 3% white male nonsmokers.

It is slowly increasing in incidence primarily due to the increase in cigarette smoking and environmental pollution. Another contributing factor is decreasing mortality from other causes such as cardiovascular and infectious diseases. Genetic factors also play a significant role in determining the possibility of airflow limitation in patients.

Emphysema severity is significantly higher in the coal worker pneumoconiosis, and this is independent of smoking status.^[1]

The exact cause of Emphysema is still yet to be distinguished, however research is suggesting the prevalence is strongly related to smoking, air pollutions and in some cases, occupation ^[3]. Another common association is the deficiency of the enzyme alpha₁-antitrypsin, which is the protein protecting the alveoli ^[4].

The prevalence of Emphysema within the smoking population is believed to increase as smoking is a major risk factor associated. It is thought to have a higher incidence in those with a lower socioeconomic background, therefore affecting lifestyle and environment, resulting in the likelihood of respiratory infection ^[5].

The alveoli and the small distal airways are primarily affected by the disease, followed by effects in the larger airways ^[4]. Elastic recoil is usually responsible for splinting the bronchioles open. However, with emphysema, the bronchioles lose their stabilizing function and therefore causing a collapse in the airways resulting in gas to be trapped distally^[4].

There is an erosion in the alveolar septa causing there to be an enlargement of the available air space in the alveoli ^[4]. There is sometimes a formation of bullae with their thin walls of diminished lung tissue.

Smoking contributes to the development of the condition initially by activating the inflammatory process ^[3]. The inhaled irritants cause inflammatory cells to be released from polymorphonuclear leukocytes and alveolar macrophages to move into the lungs ^[3]. Inflammatory cells are known as proteolytic enzymes, which the lungs are usually protected against due to the action of antiproteases such as the alpha1-antitrypsin ^[3]. However, the irritants from smoking will have an effect on the alpha1-antitrypsin, reducing its activity. Therefore emphysema develops in this situation when the production and activity of antiprotease are not sufficient to counter the harmful effects of excess protease production ^[3]. A result of this is the destruction of the alveolar walls and the breakdown of elastic tissue and collagen. The loss of alveolar tissue leads to a reduction in the surface area for gas exchange, which increases the rate of blood flow through the pulmonary capillary system ^[3].

CT scan is a common method used to diagnosis emphysema. The observations mainly seen to identify emphysema are a decrease in lung attenuation and a decrease in the number and diameter of pulmonary vessels in the affected area ^[6].

Patients diagnosed with emphysema may complain of difficult/laboured breathing and reduced exercise capacity as their predominating symptoms ^[7]. The loss of the elastic recoil in the lungs leads to irreversible bronchial obstruction and lung hyperinflation, which increases the volume over normal tidal breathing and functional residual capacity ^[7].

The main aims of treating patients with Emphysema are to relieve symptoms and to improve quality of life ^[8]^[9]. To measure patients’ quality of life, the St George’s Respiratory Questionnaire (SGRQ) and the Guyatt’s Chronic Respiratory Questionnaire (CRQ) are often completed in order to measure the effectiveness of a treatment intervention ^[8].

Other outcome measures relevant include:

6 minute walk test

Grip strength

Borg RPE

30 second sit to stand

Generally, the diagnosis for Emphysema can be based on clinical, functional and radiographic findings ^[10]. However, it is thought that mild Emphysema is not well detected on conventional chest radiography, therefore the use of pulmonary function tests (PFT) are often used to try and diagnose the condition ^[11].

In order to accurately diagnose Emphysema, the history of the patient’s condition needs to be fully understood ^[12] . The use of high-resolution CT scans is part of the standard procedure when trying to detect this condition as it is non-invasive and is found to be sensitive in detecting pathological changes related to Emphysema ^[12].

Physiotherapy and Other Management[edit | edit source]

Physiotherapy management for Emphysema is commonly associated with similar management of COPD. The use of a pulmonary rehabilitation programme consisting of exercise and education can be designed by the physiotherapist along with other members of the multi-disciplinary team (MDT) in order to maximise the patients exercise capacity, mobility and also self-confidence ^[4]. The other MDT members can consist of a respiratory nurse and dietitians, as well as the physiotherapist in the hope to treat each patient like an individual and meet their specific needs by tailoring a programme to suit them ^[4].

Pulmonary rehabilitation for patients with severe symptoms and multiple exacerbations reduces dyspnea and hospitalizations. ^[1]

As COPD is the umbrella term used for diseases like Emphysema, the prevention strategies are very similar. The most common suggestion for preventing emphysema, and such, is to stop smoking, and to avoid breathing in any harmful pollutants ^[13].

↑ ^1.0^1.1^{1. 2} Pahal P, Avula A, Sharma S. Emphysema. [Updated 2021 Feb 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-.Available: https://www.ncbi.nlm.nih.gov/books/NBK482217/#!po=74.0000(accessed 24.5.2021p
↑ ^2.0^2.1^2.2 Hochhegger B, Dixon S, Screaton N, Cardinal V, Marchiori S, Binukrishnan S, Holemans J, Gosney J, McCann C, Emphysema and smoking related lung diseases. The British Institute of Radiology 2014; 20 (4).
↑ ^3.0^3.1^3.2^3.3^3.4^3.5 Mattison S, Christensen M. The pathophysiology of emphysema: Considerations for critical care nursing practice. Intensive and Critical Care Nursing 2006; 22: 329-337.
↑ ^4.0^4.1^4.2^4.3^4.4^4.5 Hough A. Physiotherapy in respiratory and cardiac care. Hampshire: Cengage Learning EMEA, 2014
↑ Haas F, Haas SS. The Chronic Bronchitis and Emphysema Handbook. Chichester: John Wiley and Sons, Inc; 2000.
↑ Newell, J. CT of Emphysema. Radiologic Clinics of North America 2002; 40 (1): 31-42.
↑ ^7.0^7.1 Visca D, Aiello M, Chetta A. Cardiovascular function in pulmonary emphysema. BioMed Research International 2013.
↑ ^8.0^8.1 Harper R, Brazierm JE, Waterhouse JC, Walters SJ, Jones NMB, Howard P.Comparison of outcome measures for patients with chronic obstructive pulmonary disease (COPD) in an outpatient setting. Thorax 1997; 52: 879-887.
↑ Naunheim KS, Wood DE, Mohsenifar Z, Sternberg AL, Criner GJ, DeCamp MM, Deschamps CC, Martinez FJ, Sciurba FC, Tonascia J, Fishman AP. Long-term follow-up of patients receiving lung-volume-reduction surgery versus medical therapy for severe emphysema by the national emphysema treatment trial research group. The Annals of Thoracic Surgery 2006; 82 (2): 421-443.
↑ Klein JS, Gamsu G, Webb WR, Golden JA, Muller NL. High-resolution CT diagnosis of emphysema in symptomatic patients with normal chest radiographs and isolated low diffusing capacity. Radiology 1992; 182: 817-821.
↑ Sanders C, Nath PH, Bailey WC. Detection of Emphysema with computed tomography correlation with pulmonary function tests and chest radiography. Investigative Radiology 1988; 23: 262-266.
↑ ^12.0^12.1 Zaporozhan J, Ley S, Eberhardt R, Weinheimer O, Svitlana I, Herth F, Kauczor H-U. Paired inspiratory/expiratory volumetric thin-slice CT scan for emphysema analysis: comparison of different quantitative evaluations and pulmonary function test. American College of Chest Physicians 2005; 128 (5): 3212-3220.
↑ National Health Service. NHS Choices. http://www.nhs.uk/Conditions/Chronic-obstructive-pulmonary-disease/Pages/Introduction.aspx (accessed 02 June 2015)

Emphysema – Physiopedia

There are three types of emphysema; centriacinar, panacinar, paraseptal. See image 1.

Centriacinar emphysema affects the alveoli and airways in the central acinus, destroying the alveoli in the walls of the respiratory bronchioles and alveolar ducts ^[2] .
Panacinar emphysema affects the whole acinus ^[2] .
Paraseptal emphysema is believed to be the basic lesion of pulmonary bullous disease ^[2].

The prevalence of emphysema:

In United States is approximately 14 million, which includes 14% white male smokers and 3% white male nonsmokers.

Emphysema severity is significantly higher in the coal worker pneumoconiosis, and this is independent of smoking status.^[1]

Other outcome measures relevant include:

6 minute walk test

Grip strength

Borg RPE

30 second sit to stand

Physiotherapy and Other Management[edit | edit source]

Pulmonary rehabilitation for patients with severe symptoms and multiple exacerbations reduces dyspnea and hospitalizations. ^[1]

↑ ^1.0^1.1^1.2 Pahal P, Avula A, Sharma S. Emphysema. [Updated 2021 Feb 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-.Available: https://www.ncbi.nlm.nih.gov/books/NBK482217/#!po=74.0000(accessed 24.5.2021p
↑ ^2.0^2.1^2.2 Hochhegger B, Dixon S, Screaton N, Cardinal V, Marchiori S, Binukrishnan S, Holemans J, Gosney J, McCann C, Emphysema and smoking related lung diseases. The British Institute of Radiology 2014; 20 (4).
↑ ^3.0^{3. 1}^3.2^3.3^3.4^3.5 Mattison S, Christensen M. The pathophysiology of emphysema: Considerations for critical care nursing practice. Intensive and Critical Care Nursing 2006; 22: 329-337.
↑ ^4.0^4.1^4.2^4.3^4.4^4.5 Hough A. Physiotherapy in respiratory and cardiac care. Hampshire: Cengage Learning EMEA, 2014
↑ Haas F, Haas SS. The Chronic Bronchitis and Emphysema Handbook. Chichester: John Wiley and Sons, Inc; 2000.
↑ Newell, J. CT of Emphysema. Radiologic Clinics of North America 2002; 40 (1): 31-42.
↑ ^7.0^7.1 Visca D, Aiello M, Chetta A. Cardiovascular function in pulmonary emphysema. BioMed Research International 2013.
↑ ^8.0^8.1 Harper R, Brazierm JE, Waterhouse JC, Walters SJ, Jones NMB, Howard P.Comparison of outcome measures for patients with chronic obstructive pulmonary disease (COPD) in an outpatient setting. Thorax 1997; 52: 879-887.
↑ Naunheim KS, Wood DE, Mohsenifar Z, Sternberg AL, Criner GJ, DeCamp MM, Deschamps CC, Martinez FJ, Sciurba FC, Tonascia J, Fishman AP. Long-term follow-up of patients receiving lung-volume-reduction surgery versus medical therapy for severe emphysema by the national emphysema treatment trial research group. The Annals of Thoracic Surgery 2006; 82 (2): 421-443.
↑ Klein JS, Gamsu G, Webb WR, Golden JA, Muller NL. High-resolution CT diagnosis of emphysema in symptomatic patients with normal chest radiographs and isolated low diffusing capacity. Radiology 1992; 182: 817-821.
↑ Sanders C, Nath PH, Bailey WC. Detection of Emphysema with computed tomography correlation with pulmonary function tests and chest radiography. Investigative Radiology 1988; 23: 262-266.
↑ ^12.0^12.1 Zaporozhan J, Ley S, Eberhardt R, Weinheimer O, Svitlana I, Herth F, Kauczor H-U. Paired inspiratory/expiratory volumetric thin-slice CT scan for emphysema analysis: comparison of different quantitative evaluations and pulmonary function test. American College of Chest Physicians 2005; 128 (5): 3212-3220.
↑ National Health Service. NHS Choices. http://www.nhs.uk/Conditions/Chronic-obstructive-pulmonary-disease/Pages/Introduction.aspx (accessed 02 June 2015)

Emphysema – Physiopedia

There are three types of emphysema; centriacinar, panacinar, paraseptal. See image 1.

Centriacinar emphysema affects the alveoli and airways in the central acinus, destroying the alveoli in the walls of the respiratory bronchioles and alveolar ducts ^[2] .
Panacinar emphysema affects the whole acinus ^[2] .
Paraseptal emphysema is believed to be the basic lesion of pulmonary bullous disease ^[2].

The prevalence of emphysema:

In United States is approximately 14 million, which includes 14% white male smokers and 3% white male nonsmokers.

Emphysema severity is significantly higher in the coal worker pneumoconiosis, and this is independent of smoking status. ^[1]

Other outcome measures relevant include:

6 minute walk test

Grip strength

Borg RPE

30 second sit to stand

Physiotherapy and Other Management[edit | edit source]

Pulmonary rehabilitation for patients with severe symptoms and multiple exacerbations reduces dyspnea and hospitalizations. ^[1]

↑ ^1.0^1.1^1.2 Pahal P, Avula A, Sharma S. Emphysema. [Updated 2021 Feb 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-.Available: https://www.ncbi.nlm.nih.gov/books/NBK482217/#!po=74.0000(accessed 24.5.2021p
↑ ^2.0^2.1^2.2 Hochhegger B, Dixon S, Screaton N, Cardinal V, Marchiori S, Binukrishnan S, Holemans J, Gosney J, McCann C, Emphysema and smoking related lung diseases. The British Institute of Radiology 2014; 20 (4).
↑ ^3.0^3.1^3.2^3.3^3.4^3.5 Mattison S, Christensen M. The pathophysiology of emphysema: Considerations for critical care nursing practice. Intensive and Critical Care Nursing 2006; 22: 329-337.
↑ ^4.0^4.1^4.2^4.3^4.4^4.5 Hough A. Physiotherapy in respiratory and cardiac care. Hampshire: Cengage Learning EMEA, 2014
↑ Haas F, Haas SS. The Chronic Bronchitis and Emphysema Handbook. Chichester: John Wiley and Sons, Inc; 2000.
↑ Newell, J. CT of Emphysema. Radiologic Clinics of North America 2002; 40 (1): 31-42.
↑ ^7.0^7.1 Visca D, Aiello M, Chetta A. Cardiovascular function in pulmonary emphysema. BioMed Research International 2013.
↑ ^8.0^8.1 Harper R, Brazierm JE, Waterhouse JC, Walters SJ, Jones NMB, Howard P.Comparison of outcome measures for patients with chronic obstructive pulmonary disease (COPD) in an outpatient setting. Thorax 1997; 52: 879-887.
↑ Naunheim KS, Wood DE, Mohsenifar Z, Sternberg AL, Criner GJ, DeCamp MM, Deschamps CC, Martinez FJ, Sciurba FC, Tonascia J, Fishman AP. Long-term follow-up of patients receiving lung-volume-reduction surgery versus medical therapy for severe emphysema by the national emphysema treatment trial research group. The Annals of Thoracic Surgery 2006; 82 (2): 421-443.
↑ Klein JS, Gamsu G, Webb WR, Golden JA, Muller NL. High-resolution CT diagnosis of emphysema in symptomatic patients with normal chest radiographs and isolated low diffusing capacity. Radiology 1992; 182: 817-821.
↑ Sanders C, Nath PH, Bailey WC. Detection of Emphysema with computed tomography correlation with pulmonary function tests and chest radiography. Investigative Radiology 1988; 23: 262-266.
↑ ^12.0^12.1 Zaporozhan J, Ley S, Eberhardt R, Weinheimer O, Svitlana I, Herth F, Kauczor H-U. Paired inspiratory/expiratory volumetric thin-slice CT scan for emphysema analysis: comparison of different quantitative evaluations and pulmonary function test. American College of Chest Physicians 2005; 128 (5): 3212-3220.
↑ National Health Service. NHS Choices. http://www.nhs.uk/Conditions/Chronic-obstructive-pulmonary-disease/Pages/Introduction.aspx (accessed 02 June 2015)

3. Anatomy and Physiology of Breathing

It is important to understand the normal anatomy and physiology of breathing in order to identify the causes and results of COPD. Understanding the pathophysiology of ventilation will also help you understand the mechanisms of action of the pharmacologic interventions designed to open the airways.

Anatomy of the Lungs

The respiratory system is divided into the upper airway and the lower airway. The upper airway includes the nose, nasal and oral pharynx, epiglottis, and larynx (also known as the “voice box” or “Adam’s apple”). Below the larynx is the lower airway, consisting of the trachea, bronchus, and bronchiole tubes, which further divide like branches of a tree into smaller bronchioles and then end with small air sacs called alveoli.

The human body has two lungs in the thoracic cavity; there are two lobes on the left, with a border to fit the heart, and three lobes on the right side of the chest. The diaphragm divides the thoracic cavity from the abdominal cavity and is the primary muscle of respiration. Accessory muscles that help open the thoracic cavity include the internal and external intercostals of the ribs plus the abdominal muscles. When the diaphragm contracts it pulls the lungs downward, enlarging the thoracic cavity and allowing the lungs to expand and draw in air through the mouth and nose, down the trachea, larynx, and bronchi.

At the alveolar level, capillaries, the smallest vessel that connects arteries and veins, surround the alveoli and exchange oxygen for carbon dioxide. When the bronchioles and alvioli become constricted, full of mucus and less able to expand and dilate, air becomes trapped and gases are not exchanged. This creates a pressure that can make the lungs stiff and unpliable, causing the resultant barrel chest seen in many patients with COPD.

Source: Wikimedia Commons.

Physiology of Breathing

The internal pressure in the thoracic cavity is negative compared to the positive atmospheric (air) pressure. When the diaphragm contracts it opens up the thoracic cavity, allowing air to rush into the bronchioles and fill the alveoli. When the pressure within the lungs exceeds the external pressure by filling to capacity with air, the reverse occurs. The diaphragm relaxes and air is pushed out of the lungs in an exhale. COPD alters this effective function. Because the diaphragm does 80% of breathing, when the alveoli trap air, the diaphragm becomes flattened and ineffective in pulling the thoracic cavity open, which further reduces the incoming air flow.

The tissue of the bronchiole tubes contain two major receptors for the nervous system—the muscarinic and beta receptors. Muscarinic receptors cause smooth-muscle contraction, making the lumen (opening) of the bronchiole tube smaller. In contrast, the beta receptors cause relaxation of the muscle and thus bronchodilation. Ideally, the goal for people with COPD is to increase beta receptor activity (dilation of airways) and inhibit muscarinic receptors. The two main classes of medications act on these receptors. Because people with COPD also have inflammation of the airways, a third major pharmacologic mechanism to change this cycle of airway over-reactivity is an anti-inflammatory such as inhaled corticosteroids.

Obstructive and Restrictive Lung Disease

COPD results when there is a chronic obstruction or restriction of full air flow. The obstruction is generally mucus, whereas the restriction is the narrowing of the bronchioles or alveoli. Asthma often results in a restrictive airway as environmental triggers create a spasm of the bronchioles resulting in bronchoconstriction.

COPD is caused by a bronchoconstriction and inflammation, making air passage in and out of the lungs more difficult. This reduction in effective air flow creates a state of hypoxia, resulting in hypoxemia. As noted earlier, chronic bronchitis is a chronic productive cough lasting 3 months during 2 consecutive years. Emphysema is a permanent enlargement of the alveoli, which prevents normal elastic recoil during respiration.

People with asthma develop an obstruction of the airway and air flow. Those with asthma who have a reversible air flow obstruction are not considered to have COPD; however, when the air flow remains chronically obstructed, and is not reversible, they are diagnosed with COPD (Jarvis, 2015).

The lungs become scarred from chronic inflammation and irritation caused by mucus buildup as the lungs attempt to protect themselves from environmental irritants such as smoke. This cycle of irritation, inflammation, and attempts at recovery continue until the compensation efforts create disruptive symptoms that drive the patient to seek medical care. A productive cough with mucus is an effort of the lungs and trachea to rid themselves of the irritant; however, the mucus may soon become a problem in itself, and is sometimes known as a “smoker’s cough.”

Effects of Smoking

[Material in this section is from smokefree.gov 2018 unless otherwise cited.]

Smoking, the number one cause of COPD, destroys the cilia (fine hairs) in the bronchiole tubes and trachea that are supposed to push foreign substances and pathogens from the lower airway into the upper airway so they can be expelled by a cough. Pathology from smoking affects not only the lungs but also the circulatory system (Glass, 2014). Nicotine paralyzes the cilia, and the tar within cigarettes or cigars further destroys their integrity.

Additionally, the chemicals in cigarette smoke create nicks within the fine endothelial lining of the arteries throughout the body, leaving places for cholesterol and fat to build up. Generally, the public is aware of cigarette smoking as the most common cause of lung cancer; however, most people are unaware of the damage to the circulatory system, which is also the most common cause of atherosclerosis, or narrowing of the arteries.

Further, nicotine competes with oxygen in the formation of new red blood cells, which can lead the blood to become thick and sticky, forming atherosclerotic plaques that narrow arteries and hinder blood flow. The surface of a bulging atherosclerotic plaque sometimes tears, exposing material that stimulates clot formation. Clots and ruptured plaque material can then break away from the wall, be carried by the blood, and clog arteries downstream.

Atherosclerosis can damage tissues throughout the body:

Blockages in the carotid arteries can reduce or block blood flow to the brain, causing a stroke.
Obstructions in the peripheral arteries in the legs can cause claudication (pain when walking) gangrene, and deep vein thrombosis (DVT).
Resultant DVTs can travel to the lungs, causing a pulmonary embolism and respiratory arrest.
Atherosclerotic obstructions in the intestines cause ischemic bowel.
In the coronary arteries, atherosclerotic obstructions cause heart attacks. (NHLBI, 2016)

Smoking affects each body system as it reduces the oxygen supply to tissues and cells. Within the brain it becomes an addictive substance, as strong as heroin. Nicotine and tar reduce the oxygen supply to the cochlea of the inner ear, causing hearing loss, and retinas of the eyes, which may lead to macular degeneration and blindness. The loss of skin elasticity due to smoking can lead to accelerated wrinkles, dull skin tone, and dryness.

At the cellular level, DNA is disrupted by the nicotine and tars from smoking, which can lead to uncontrolled mutations in cellular replication known as cancer. One-third of all cancer deaths are caused by tobacco and smoking. Cancers of the mouth and throat are caused by smoking. In addition to disruptions in normal DNA creation of proteins, hormones disruptions result in lowered estrogen and testosterone levels, thyroid problems, and reproduction issues.

Alveoli of Smoker and Non-Smoker

Upper right: This image shows the clear pink alveoli of a non-smoker without COPD; lower right: this image reveals the hyperinflation and clogging of the alveoli from COPD, which makes gas exchange much less effective.
Source: Wikimedia Commons.

Within the circulatory system, both white and red blood cell counts stay elevated in smokers. High white blood cell counts indicate that the body is in a state of infection, a continuing cycle of inflammation with attempts to repair itself. Overproduction of red blood cells in the bone marrow places stress on other body systems. In the skeletal system there is a higher risk for osteoporosis (loss of bone density), which can lead to fractures. Muscle pains and weakness are more common among smokers that non-smokers. Healing bones, muscles, and skin take much longer without adequate oxygen.

Although electronic cigarettes (“vapes”) may eliminate the tars found in traditional cigarettes and cigars, their nicotine still causes detrimental effects on each of the body systems. The FDA has not approved electronic cigarettes for a smoking cessation strategy due to the similar adverse effects of nicotine.

In addition to the nicotine, manufacturers have added heavy metals and other debris, chemicals, fuels, and flavorings (including formaldehyde, used in embalming a corpse) to their products with each of their own adverse effects on the body.

According to Stanton Glantz, who directs the UCSF Center for Tobacco Control Research and Education,

E-cigarettes are widely promoted as a smoking cessation aid but for most people they actually make it harder to quit smoking; so, most people end up as so-called dual users who keep smoking while using e-cigarettes. The new study shows that the risks compound. Someone who continues to smoke daily while using e-cigarettes daily has an increased risk of a heart attack by a factor of five. (LaMotte & Scutti, 2018)

Mark has discovered that the result of 20 years of smoking has compromised his lungs’ ability to inhale and exhale. Unfortunately, his symptoms of shortness of breath and persistent cough were his only indicators. Mark’s provider will order additional diagnostic studies to confirm the diagnosis, including a spirometry, lab tests to establish a baseline, and a chest x-ray.

Test Your Learning

What is the pathology of COPD within the bronchioles?

The bronchioles are not affected, but the alveoli become hyperinflated.
The bronchioles become constricted and often are full of mucus.
The bronchioles become expanded and the alveoli constrict.
The cilia within the trachea become elongated to compensate for the closing airways.

Apply Your Knowledge

What can you teach people who smoke about the effects of smoking on their lungs and arteries?

Answer: B

Emphysema – StatPearls – NCBI Bookshelf

Continuing Education Activity

Pulmonary emphysema, a progressive lung disease, is a form of chronic obstructive pulmonary disease (COPD). Global Initiative for Chronic Obstructive Lung Disease (GOLD) defines it as “a common, preventable and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases.” This activity reviews the cause, pathophysiology, and presentation of emphysema and highlights the role of the interprofessional team in its management.

Objectives:

Review the causes of emphysema.
Describe the pathophysiology of emphysema.
Summarize the treatment of emphysema.
Outline the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected by emphysema.

Earn continuing education credits (CME/CE) on this topic.

Introduction

Pulmonary emphysema, a progressive lung disease, is a form of chronic obstructive pulmonary disease (COPD). The Global Initiative for chronic obstructive lung disease (GOLD) has defined COPD as “a common, preventable, and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases.”[1][2][3]

COPD is the third leading cause of death in the United States and the fourth leading cause of death worldwide. The World Health Organization (WHO) estimates suggest that it will rise to be the third most common cause of death worldwide by 2020. COPD includes patients with chronic bronchitis and emphysema. Although identified as separate entities, most patients with COPD have features of both. COPD often coexists with comorbidities, which affect the disease course.

Emphysema is primarily a pathological diagnosis that affects the air spaces distal to the terminal bronchiole. It is characterized by abnormal permanent enlargement of lung air spaces with the destruction of their walls without any fibrosis and destruction of lung parenchyma with loss of elasticity.

Etiology

Emphysema is caused by chronic and significant exposure to noxious gases, of which cigarette smoking remains the most common cause, and 80% to 90% of patients with COPD are cigarette smokers identified, with 10% to 15% smokers developing COPD. However, in smokers, the symptoms also depend on the intensity of smoking, years of exposure, and baseline lung function. oms usually begin after at least 20 packs per year of tobacco exposure.[4][5]

Biomass fuels and other environmental pollutants such as sulfur dioxide and particulate matter are recognized as an important cause in developing countries affecting women and children greatly. A rare hereditary autosomal recessive disease, alpha one antitrypsin deficiency, can also lead to emphysema and liver abnormalities. However, it only contributes to 1% to 2% of cases of COPD. It is a proven risk factor and can present with pan-acinar bibasilar emphysema early in life.

Other etiological factors are passive smoking, lung infections, and allergies. Moreover, low birth weight as a newborn makes one more prone to develop COPD later in life.

Epidemiology

The prevalence of emphysema in the United States is approximately 14 million, which includes 14% white male smokers and 3% white male nonsmokers. The prevalence is slightly less for white female smokers and African Americans. These patient groups tend to develop emphysema after less exposure time than other patient populations.

Emphysema severity is significantly higher in the coal worker pneumoconiosis, and this is independent of smoking status.

Pathophysiology

The clinical manifestations of emphysema are the consequences of damage to airways distal to terminal bronchiole, which include respiratory bronchiole, alveolar sacs, alveolar ducts, and alveoli, collectively known as the acinus. There is abnormal permanent dilatation of the airspaces and destruction of their walls due to the action of the proteinases. This results in a decrease in the alveolar and the capillary surface area, which decreases the gas exchange. The part of the acinus affected determines the subtype.

It can be subdivided pathologically into the following:

Centrilobular (proximal acinar) is the most common type and is commonly associated with smoking. It can also be seen in coal workers’ pneumoconiosis.
Panacinar is most commonly seen with alpha one antitrypsin deficiency.
Paraseptal (distal acinar) may occur alone or in association with the above two. When it occurs alone, the usual association is a spontaneous pneumothorax in a young adult.

After long-term exposure to noxious smoke, inflammatory cells such as macrophages, neutrophils, and T lymphocytes are recruited, which play an important role in the development of emphysema. First, macrophages are activated, which release neutrophil chemotactic factors like leukotriene B4 and interleukin-8. Once the neutrophils are recruited, these, along with macrophages, release multiple proteinases and lead to mucus hypersecretion.

Elastin is an important component of the extracellular matrix that is required to maintain the integrity of lung parenchyma and small airways. Elastase/anti-elastase imbalance increases the susceptibility to lung destruction leading to airspace enlargement. Cathepsins and neutrophil-derived proteases (i.e., elastase and proteinase) act against elastin and destroy the connective tissue of the parenchyma of the lung. Cytotoxic T cells release TNF-a and perforins, which destroy the epithelial cells of the alveolar wall.

Cigarette smoking not only causes mucus hypersecretion and release of neutrophilic proteolytic enzymes, but it also inhibits anti-proteolytic enzymes and alveolar macrophages. Genetic polymorphisms have a role in inadequate antiproteases production in smokers. All of these contribute to the development of emphysema.

Lung parenchyma produces alpha one antitrypsin (AAT), which inhibits trypsinize and neutrophil elastase in the lung. AAT deficiency can lead to panacinar emphysema.

History and Physical

Most patients present with very nonspecific symptoms of chronic shortness of breath and cough with or without sputum production. As the disease process advances, the shortness of breath and cough progressively gets worse. Initially, there is exertional dyspnea with significant physical activity, especially arm work at or above shoulder level with progression to dyspnea with simple daily activities and even at rest. Some patients may present with wheezing because of the airflow obstruction.

As COPD advances, patients can lose significant body weight due to systemic inflammation and increased energy spent in the work of breathing. Also, there are frequent intermittent exacerbations as the obstruction of the airways increases. Episodes of COPD exacerbations may present with increased shortness of breath, increased severity of a cough, and increased sputum typically brought on by an infection or an environmental factor.

Smoking history is important, with an emphasis on the age at which the person started smoking and the total pack years. If the person has quit smoking, it is important to know how many years have passed since he/she last smoked. History of environmental and occupational exposure and family history of chronic respiratory conditions and COPD is essential.

In the early stages of the disease, the physical examination may be normal. Patients with emphysema are typically referred to as “pink puffers,” meaning cachectic and non-cyanotic. Expiration through pursed lips increases airway pressure and prevents airway collapse during respiration, and the use of accessory muscles of respiration indicates advanced disease. Clubbing of the digits is not typical of COPD. Many other comorbidities may be possible. Current smokers may have an odor of smoke and nicotine staining of hands and fingernails.

Percussion may be normal early in the disease. The rest of the examination may range from prolonged expiration or wheezes on forced exhalation to increased resonance, indicating hyperinflation as the airway obstruction increases. Distant breath sounds, wheezes, crackles at the lung bases, and/or distant heart sounds are heard on auscultation.

Evaluation

Emphysema is a pathological diagnosis. Accordingly, routine laboratory and radiographic studies are not indicated.

Pulmonary function testing (PFT), particularly spirometry, is the mainstay of diagnosis. A post-bronchodilator test may be done in those with abnormal values. COPD is only partially reversible or irreversible with a bronchodilator, and post-bronchodilator FEV1/FVC is less than 0.07, which is diagnostic.[8][9][10][11]

GOLD staging based on the severity of airflow limitation is as follows:

Mild with FEV1 greater or equal to 80% predicted
Moderate with FEV1 less than 80% predicted
Severe with FEV1 less than 50% predicted
Very severe with FEV1 less than 30% predicted

The lung volume measurements indicative of air trapping in emphysema reveal increased residual volume and total lung capacity. Diffusing capacity for carbon monoxide is reduced due to the emphysematous destruction of the alveolar-capillary pulmonary membrane.

A chest x-ray is only helpful in diagnosis if emphysema is severe, but it is usually the first step when suspecting COPD to rule out other causes. Destruction of alveoli and air trapping causes hyperinflation of the lungs with flattening of the diaphragm, and the heart appears elongated and tubular in shape.

Arterial blood gases are usually not required in mild to moderate COPD. It is done when oxygen saturation goes below 92% or when an assessment of hypercapnia is needed in severe airflow obstruction.

A young person with symptoms of emphysema should be tested for alpha 1 antitrypsin deficiency (AATD).

Treatment / Management

There is no known, definitive treatment that can modify the disease process. However, risk-factor modification and management of symptoms have been proven effective in slowing the disease progression and optimizing the quality of living.[12][13][14]

Based on the symptoms and number of exacerbations, we can divide the disease into 4 COPD GOLD stages and modify the treatment accordingly.

Medical Therapy

Medical therapy includes using a bronchodilator alone or in combination with anti-inflammatory drugs such as corticosteroids and phosphodiesterase-4 inhibitors.

Bronchodilator

The primary mechanisms of action can be divided into two categories: beta2 agonists and anticholinergic medications. They are first-line drugs for COPD and are administered by inhalation. They are known to improve FEV1 by altering the smooth muscle tone of the airways and thus improving exercise tolerance. Bronchodilators are usually given regularly to prevent and reduce symptoms, exacerbations, and hospitalizations.

Short-acting beta2 agonists (SABA) and short-acting muscarinic antagonists (SAMA) are usually prescribed as needed for the management of intermittent dyspnea. Long-acting beta2 agonists (LABA) and long-acting muscarinic antagonists (LAMA) are used, especially in cases of increasing dyspnea or more than occasional dyspnea. If the symptoms are persistent while on one bronchodilator, another bronchodilator should be added.

Beta2 agonists cause relaxation of airway smooth muscles. SABA, like albuterol, can be used with or without anticholinergics. SABA is the mainstay in COPD exacerbation. LABA includes formoterol, salmeterol, indacaterol, olodaterol, vilanterol, among others. The side effects are arrhythmias, tremors, and hypokalemia. Caution should be taken in heart failure as tachycardia may precipitate heart failure.

Anticholinergics inhibit acetyl-choline-induced bronchoconstriction. SAMA includes ipratropium and oxitropium. LAMA, such as tiotropium, can be given once daily.

Inhaled corticosteroid (ICS) is an add-on therapy to bronchodilator in a step-up therapy. ICS includes beclomethasone, budesonide, fluticasone, etc. The common side effects are local infection, cough, and pneumonia. Oral systemic corticosteroids are used for all patients with COPD exacerbation and avoided in stable patients due to more adverse effects.

Oral Phosphodiesterase-4 inhibitors like roflumilast act by reducing inflammation and can be added if there is severe airflow obstruction with no improvement with the above medications.

Triple inhaled therapy (LABA+ LAMA+ ICS) has been recently approved by the FDA and is taken only once a day.

Intravenous alpha1 antitrypsin augmentation therapy for AATD patients. The high cost and lack of availability is the main limitation of this therapy.

Supportive Therapy

Supportive therapy includes oxygen therapy and ventilatory support, pulmonary rehabilitation, and palliative care.

Routine supplemental oxygen does not improve the quality of life or clinical outcomes in stable patients. Continuous long-term, i.e., longer than 15 hours of supplemental oxygen, is recommended in patients with COPD with PaO2 less than 55 mmHg (or oxygen saturation less than 88%) or PaO2 less than 59 mm Hg in case of cor pulmonale. Oxygen therapy has been shown to increase the survival of these patients with severe resting hypoxemia. For those who desaturate with exercise, intermittent oxygen will help. The goal is to maintain oxygen saturation greater than 90%.

A major cause of hypoxemia in COPD is due to ventilation-perfusion mismatch (V/Q mismatch), particularly in low V/Q areas. Hypoxic vasoconstriction of pulmonary arteries is to improve overall gas exchange efficiency. Supplemental oxygen can successfully reach the alveoli in these lungs, which prevents this vasoconstriction and thereby increases perfusion and improves gas exchange, thus resulting in improvement of hypoxemia.

Noninvasive positive pressure ventilation (NPPV) is known to decrease morbidity and mortality in patients with acute respiratory failure. It should be tried as the first mode of ventilation in patients with COPD exacerbation with respiratory failure who otherwise have no absolute contraindication as it improves gas exchange, decreases hospitalization duration, reduces work of breathing, improves VQ matching, and improves survival. If NPPV does not work in a patient with COPD in a hospital setting, the patient should be intubated and put on a ventilator.

Pulmonary rehabilitation for patients with severe symptoms and multiple exacerbations reduces dyspnea and hospitalizations and is recommended for GOLD stages B, C, and D.

Although available from the time the person is diagnosed with COPD, palliative care is typically recommended for GOLD stage D. It is additional care to the patient’s ongoing treatment plan. The goal is to provide the best quality of life possible. Not only does it play a role in the assessment and management of the symptoms, but it also helps patients understand their illness and facilitates a discussion about the patient’s goal of care, advance care, and end-of-life care plans. Advance care planning involves communication between patients, their families, and the physician and helps patients formulate their treatment preferences. Reassuring patients with a clear plan to deal with dyspnea in advanced disease and management of depression and anxiety is an important component of palliative care. These can be managed with low-dose opioids, lifestyle modification, and relaxation techniques, respectively. Most patients underestimate the disease, so it is important to look for transition time and discuss advanced care early in the disease. It is also important to explore where the patients want to spend their last days (e.g., home or hospital) and help provide them with as much comfort as possible.

Interventional Therapy

Additional Interventions

Identification and reduction of exposure to risk factors. Counseling about smoking cessation is the single most important intervention that slows the progression of the disease. Reducing the exposure to open cooking fires and promoting efficient ventilation also benefits.
Daily oral opioids for severe COPD symptoms refractory to medical therapy. Nutritional supplementation in malnourished patients with COPD
Pneumococcal vaccine 23 valent every five years for patients with COPD older than 65 or with other cardiopulmonary disease and Influenza vaccine for all patients with COPD every year
Readmission rates can be reduced with counseling on the optimal use of metered-dose inhalers (MDI)
Exercise for all patients with COPD

Management of a Patient with COPD Exacerbation

Beta-blockers and anticholinergics are used simultaneously. Initially with nebulizers and later switched to MDI. Systemic corticosteroids (intravenous or oral) are shown to hasten recovery and decrease hospital stay. Antibiotics are beneficial, especially if a cough productive of purulent sputum is present. Second generation macrolides, extended-spectrum fluoroquinolones, cephalosporins, and amoxicillin-clavulanate. NIPPV can be beneficial in patients who can protect their airway and do not have a major acid-base disorder on the ABG. Very often, patients with end-stage COPD with exacerbations are intubated and are put on a ventilator. Ventilated patients should be watched for the development of auto-PEEP and its related complications.

Prevention

Smoking cessation
Vaccination against Pneumococcus and Haemophilus Influenzae.[15][16]

Differential Diagnosis

The disease presents with nonspecific symptoms, and hence, it has broad differential diagnoses. These include:

Chronic obstructive asthma
Chronic bronchitis with normal spirometry
Cystic fibrosis
Bronchopulmonary mycosis
Central airway obstruction
Bronchiectasis
Heart failure
Tuberculosis
Constrictive bronchiolitis
Anemia
Complications
Pulmonary hypertension
Cor pulmonale
Chronic respiratory failure
Spontaneous pneumothorax

Prognosis

Various prognostic indicators have been evaluated with regard to mortality and morbidity associated with emphysema. Following measures have been correlated with the disease burden and prognosis:

The coexistence of other illnesses also makes the prognosis poorer in COPD patients. For instance, patients with features of both asthma and COPD have a poorer quality of life with higher mortality rates. Similarly, patients with emphysema who have raised serum alpha-1 antitrypsin levels also have higher mortality.[18] Other frequently encountered comorbid illnesses include metabolic syndrome, cardiovascular disease, hypertension, and bronchiectasis.[19]

A widely used tool for prognosis prediction is the BODE index which takes into account the following:

BMI
FEV (obstruction)
Dyspnea
Exercise capacity

Complications

Patients suffering from emphysema are prone to develop various complications, some of which are life-threatening. Following are some most frequently encountered complications of emphysema:

Respiratory insufficiency or failure
Pneumonia
Pneumothorax
Chronic atelectasis
Cor pulmonale
Interstitial emphysema
Recurrent respiratory tract infections
Respiratory acidosis, hypoxia, and coma

Consultations

An internist, an emergency physician, a pulmonary specialist, specialized nurses, respiratory therapists, and physician assistants all need to play their part in the management of patients with emphysema. A pulmonary specialist’s help is to be sought in the following cases:

When the diagnosis is uncertain
Persistent symptoms despite initial medical therapy
Frequent exacerbations despite medical management
ATTD is diagnosed
Atypical presentation
Alarming features (hemoptysis, weight loss, night sweats)
Coexistence of asthma and COPD
Other comorbid illnesses

Pearls and Other Issues

Medications for primary pulmonary hypertension are not recommended for patients with pulmonary hypertension secondary to COPD.
Depression and anxiety are very common in end-stage lung disease, and pharmacological agents can be used accordingly.
Statin therapy does not reduce exacerbation.
Long-term oral corticosteroids are not recommended.
ICS alone is not recommended.
Combination treatment with LABA and LAMA is more effective in reducing exacerbations as compared to monotherapy.
A combination of SAMA and SABA improves symptoms and FEV-1.
Theophylline has a little bronchodilator effect in stable COPD and is associated with modest symptomatic benefits.
Assessment and appropriate management for comorbidities in a patient with COPD independently influence mortality and hospitalizations.
Excessive correction of hypoxia in a patient with longstanding COPD can sometimes lead to hypercapnia. This is due to the loss of compensatory vasoconstriction with an ineffective gas exchange as there is a loss of hypoxic drive for ventilation. Also, increased oxyhemoglobin decreases the uptake of carbon dioxide due to the Haldane effect.
The only interventions that decrease the mortality of COPD are smoking cessation and continuous home oxygen.

Enhancing Healthcare Team Outcomes

The management of emphysema is by an interprofessional team that consists of a pulmonologist, internist, pharmacist, dietitian, social worker, respiratory therapist, primary care provider, and a thoracic surgeon. There is no cure for emphysema, and the primary cause needs to be treated. This means educating the patient about the harms of smoking and getting the annual influenza vaccine. The outlook for most patients is guarded, and the quality of life is poor, marked by frequent exacerbations and remissions of acute respiratory distress. Some may develop repeated pneumothoraces, which may need to be managed by a thoracic surgeon. Several types of lung volume reduction procedures are available, but they are high risk, associated with serious complications, and require prolonged intensive care. Pharmacists must review prescriptions, check for interactions, and stress the importance of compliance to patients and their families. Nurses should monitor and educate patients, reporting changes in status to the team.[2][20] [Level 5]

Continuing Education / Review Questions

Figure

CT Scan, COPD, Chronic Obstructive Pulmonary Disease, Paraseptal Emphysema. Contributed by chestatlas.com (H. Shulman MD)

Figure

X-ray, COPD, Chronic Obstructive Pulmonary Disease, Subtle Paraseptal Emphysema. Contributed by chestatlas.com (H. Shulman MD)

Figure

Emphysema. Contributed by Sandeep Sharma, MD

Figure

Subcutaneous emphysema. Image courtesy S Bhimji MD

References

1.: Rustagi N, Singh S, Dutt N, Kuwal A, Chaudhry K, Shekhar S, Kirubakaran R. Efficacy and Safety of Stent, Valves, Vapour ablation, Coils and Sealant Therapies in Advanced Emphysema: A Meta-Analysis. Turk Thorac J. 2019 Jan 01;20(1):43-60. [PMC free article: PMC6340687] [PubMed: 30664426]
2.: Fernandez-Bussy S, Labarca G, Herth FJF. Bronchoscopic Lung Volume Reduction in Patients with Severe Emphysema. Semin Respir Crit Care Med. 2018 Dec;39(6):685-692. [PubMed: 30641586]
3.: Dunlap DG, Semaan R, Riley CM, Sciurba FC. Bronchoscopic device intervention in chronic obstructive pulmonary disease. Curr Opin Pulm Med. 2019 Mar;25(2):201-210. [PubMed: 30640188]
4.: Asri H, Zegmout A. [The two major complications of tobacco in a single image!] Pan Afr Med J. 2018;30:252. [PMC free article: PMC6307924] [PubMed: 30627313]
5.: Thomson NC. Challenges in the management of asthma associated with smoking-induced airway diseases. Expert Opin Pharmacother. 2018 Oct;19(14):1565-1579. [PubMed: 30196731]
6.: Zhang H, Dong L, Kang YK, Lu Y, Wei HH, Huang J, Wang X, Huang K. Epidemiology of chronic airway disease: results from a cross-sectional survey in Beijing, China. J Thorac Dis. 2018 Nov;10(11):6168-6175. [PMC free article: PMC6297443] [PubMed: 30622788]
7.: Mouronte-Roibás C, Fernández-Villar A, Ruano-Raviña A, Ramos-Hernández C, Tilve-Gómez A, Rodríguez-Fernández P, Díaz ACC, Vázquez-Noguerol MG, Fernández-García S, Leiro-Fernández V. Influence of the type of emphysema in the relationship between COPD and lung cancer. Int J Chron Obstruct Pulmon Dis. 2018;13:3563-3570. [PMC free article: PMC6214583] [PubMed: 30464438]
8.: Harrison R, Knowles S, Doherty C. Surgical Emphysema in a Pediatric Tertiary Referral Center. Pediatr Emerg Care. 2020 Jan;36(1):e21-e24. [PubMed: 30672901]
9.: Buttar BS, Bernstein M. The Importance of Early Identification of Alpha-1 Antitrypsin Deficiency. Cureus. 2018 Oct 25;10(10):e3494. [PMC free article: PMC6318138] [PubMed: 30648036]
10.: Cheng T, Li Y, Pang S, Wan HY, Shi GC, Cheng QJ, Li QY, Pan ZL, Huang SG. Emphysema extent on computed tomography is a highly specific index in diagnosing persistent airflow limitation: a real-world study in China. Int J Chron Obstruct Pulmon Dis. 2019;14:13-26. [PMC free article: PMC6301435] [PubMed: 30587958]
11.: Bhatt SP, Bhakta NR, Wilson CG, Cooper CB, Barjaktarevic I, Bodduluri S, Kim YI, Eberlein M, Woodruff PG, Sciurba FC, Castaldi PJ, Han MK, Dransfield MT, Nakhmani A. New Spirometry Indices for Detecting Mild Airflow Obstruction. Sci Rep. 2018 Nov 30;8(1):17484. [PMC free article: PMC6269456] [PubMed: 30504791]
12.: Campo MI, Pascau J, José Estépar RS. EMPHYSEMA QUANTIFICATION ON SIMULATED X-RAYS THROUGH DEEP LEARNING TECHNIQUES. Proc IEEE Int Symp Biomed Imaging. 2018 Apr;2018:273-276. [PMC free article: PMC6239425] [PubMed: 30450153]
13.: Storre JH, Callegari J, Magnet FS, Schwarz SB, Duiverman ML, Wijkstra PJ, Windisch W. Home noninvasive ventilatory support for patients with chronic obstructive pulmonary disease: patient selection and perspectives. Int J Chron Obstruct Pulmon Dis. 2018;13:753-760. [PMC free article: PMC5836655] [PubMed: 29535515]
14.: Press VG, Cifu AS, White SR. Screening for Chronic Obstructive Pulmonary Disease. JAMA. 2017 Nov 07;318(17):1702-1703. [PubMed: 29114819]
15.: Calverley PMA, Anderson JA, Brook RD, Crim C, Gallot N, Kilbride S, Martinez FJ, Yates J, Newby DE, Vestbo J, Wise R, Celli BR., SUMMIT (Study to Understand Mortality and Morbidity) Investigators. Fluticasone Furoate, Vilanterol, and Lung Function Decline in Patients with Moderate Chronic Obstructive Pulmonary Disease and Heightened Cardiovascular Risk. Am J Respir Crit Care Med. 2018 Jan 01;197(1):47-55. [PubMed: 28737971]
16.: Wood-Baker RR, Gibson PG, Hannay M, Walters EH, Walters JA. Systemic corticosteroids for acute exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2005 Jan 25;(1):CD001288. [PubMed: 15674875]
17.: Haruna A, Muro S, Nakano Y, Ohara T, Hoshino Y, Ogawa E, Hirai T, Niimi A, Nishimura K, Chin K, Mishima M. CT scan findings of emphysema predict mortality in COPD. Chest. 2010 Sep;138(3):635-40. [PubMed: 20382712]
18.: Takei N, Suzuki M, Makita H, Konno S, Shimizu K, Kimura H, Kimura H, Nishimura M. Serum Alpha-1 Antitrypsin Levels and the Clinical Course of Chronic Obstructive Pulmonary Disease. Int J Chron Obstruct Pulmon Dis. 2019;14:2885-2893. [PMC free article: PMC6911326] [PubMed: 31849461]
19.: Singh D, Agusti A, Anzueto A, Barnes PJ, Bourbeau J, Celli BR, Criner GJ, Frith P, Halpin DMG, Han M, López Varela MV, Martinez F, Montes de Oca M, Papi A, Pavord ID, Roche N, Sin DD, Stockley R, Vestbo J, Wedzicha JA, Vogelmeier C. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Lung Disease: the GOLD science committee report 2019. Eur Respir J. 2019 May;53(5) [PubMed: 30846476]
20.: Oey I, Waller D. The role of the multidisciplinary emphysema team meeting in the provision of lung volume reduction. J Thorac Dis. 2018 Aug;10(Suppl 23):S2824-S2829. [PMC free article: PMC6129798] [PubMed: 30210837]

Pathology Outlines – Emphysema

Lung

Obstructive pulmonary disease

Emphysema

Topic Completed: 1 December 2016

Minor changes: 3 June 2021

Copyright: 2003-2021, PathologyOutlines.com, Inc.

PubMed Search: emphysema[title]

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Cite this page: Yoshikawa A, Bychkov A. Emphysema. PathologyOutlines.com website. https://www.pathologyoutlines.com/topic/lungnontumoremphysema.html. Accessed August 5th, 2021.

Definition / general

Pulmonary emphysema is defined as permanent abnormal enlargement of air spaces distal to the terminal bronchioles with destruction of the alveolar septa with little or no fibrosis
In a broad sense, emphysema refers to the condition when air is abnormally introduced and trapped in the tissue; it can occur in any part of body such as subcutaneous soft tissue, mediastinum, epidural area and solid organs

Essential features

Destruction of acinar structure and airspace enlargement, especially due to cigarette smoking
Affects multiple pulmonary functions and causes chronic respiratory symptoms

Sites

Centriacinar emphysema
- Upper lobe predominant
- Respiratory bronchioles and surrounding lung parenchyma
Panacinar emphysema
- Lower lobe predominant
- Entire acinus
Paraseptal emphysema
- Upper lung
- Distal part of acinus in subpleural area

Pathophysiology

Destruction of lung parenchymal tissue due to chronic inflammation
Protease mediated destruction of elastin is an important feature (Thorax 2016;71:105)
Morphological progression (Int J Chron Obstruct Pulmon Dis 2016;11:2287, Clin Anat 2015;28:227)
- Increase in size and number of small fenestrae in alveolar walls (“pores of Kohn”), which leads to loss of elastic recoil
- Breakdown and merging of fibrovascular trabeculae (“framework”)
- Remodeling of acini results in airspace enlargement

Etiology

Inhalation
- Cigarette smoking and environmental pollutants, especially for centriacinar emphysema
- However, there is individual susceptibility (Annu Rev Physiol 2014;76:493)
Infections
Genetic factors

Clinical features

Dyspnea; chronic, progressive and usually irreversible
Chest inflation
CPFE (Chest 2012;141:222, Eur Respir J 2005;26:586)
- Coexistence of interstitial fibrosis and emphysema of unknown causes
- Patients with CPFE have different pulmonary function tests and outcomes than patients with pure emphysema or pure fibrosis
Interstitial emphysema (Am J Surg Pathol 2014;38:339)
- Air gains access to the pulmonary interstitium to cause air leak and pneumothorax
- Common in premature infants
- Adults: commonly in usual interstitial pneumonia, but can occur in any interstitial lung diseases
Bullous emphysema
- Formation of multiple bullae > 1 cm with thin wall
- Can cause bullae inflation and pneumothorax
Senile emphysema
- Due to age related alteration of acini
Irregular emphysema
- Occurs in relation to scars
Congenital lobar emphysema (Pediatr Clin North Am 1994;41:453)
- Hyperinflation of one or more lobes due to malformation of bronchioles
- Causes respiratory distress
- Can be sporadic or caused by autosomal dominant inheritance

Radiology description

X ray: overinflation of the lung, but it may not be seen in early stages
Chest CT: emphysematous regions are represented by low attenuation areas (Eur Respir J 2016;48:216)

Prognostic factors

Based on exacerbation risk of COPD (GOLD)
- GOLD score 3 or 4 (severe or very severe airflow limitation)
- Previous history of exacerbation and hospitalization
- Faster loss of forced expiratory volume in 1 sec
- COPD assessment test score ≥ 10 (CATest, Eur Respir J 2009;34:648)

Treatment

Based on treatment of COPD (GOLD)
- Smoking cessation
- Medications: bronchodilators, antimuscarinic drugs, steroids, etc.
- Ventilatory support
- Surgical interventions: lung volume reduction surgery, bullectomy, lung transplant
- Augmentation therapy for alpha-1-antitrypsin deficiency (Eur Respir Rev 2015;24:46)

Gross description

Centriacinar: sparse empty spaces with pigmentation (anthracosis) corresponding enlarged airspaces
Panacinar: airspaces are more or less evenly inflated throughout the secondary lobules
Paraseptal: inflated subpleural airspaces with thin walls

Microscopic (histologic) description

General findings
- Airspace enlargement; the size of airspace in the background parenchyma will be a good reference
- Fragmented alveolar walls
  - If the acinar arrangement is well remained, it is representing pores of Kohn
  - If not, it is representing acinar destruction
- Mild fibrotic change can be seen
- Any degrees of inflammation can accompany
- The subtype is determined with histological landmarks:
  - Bronchovascular bundle of terminal bronchiole and arteriole is in the center of acinus
  - Connective tissue septa (“secondary lobule of Millar”) are the periphery of acinus, which is often ambiguous in less inflamed lung
- Note: similar appearance can be seen due to inadequate inflation or fixation of specimen
CPFE
- Centrilobular emphysema in upper lobes
- Usual interstitial pneumonia in lower lobes
Interstitial emphysema
- Elongated or angulated spaces in fibrotic interstitium
- Surrounded by dense fibrosis and lining of multiple giant cells, but not epithelium
- Most commonly around bronchovascular bundles

Microscopic (histologic) images

Virtual slides

Images hosted on other servers:

Severe emphysema

Electron microscopy images

Images hosted on other servers:

Remodeling of elastin and collagen

Videos

Histopathology Lung – Emphysema

What Is Emphysema?

Emphysema is a type of lung disease. It limits the movement of air in and out of your lungs. This makes breathing harder. It’s most often caused by heavy, long-term cigarette smoking. Emphysema is one of a group of conditions called chronic obstructive pulmonary disease (COPD).

Healthy lungs

Inside the lungs are branching airways made of stretchy tissue. Each airway is wrapped with bands of muscle that help keep it open. Air travels in and out of the lungs through these airways.

The tubes branch into smaller passages called bronchioles . These end in clusters of balloon-like sacs called alveoli..

Blood vessels surrounding the alveoli move oxygen into the blood. At the same time, the alveoli remove carbon dioxide from the blood. The carbon dioxide is then exhaled.

When you have emphysema

Airways become damaged. When the lung tissue loses its stretchiness, the surrounding airways collapse more easily and trap air in the lungs.

Damaged airways collapse when you exhale. This causes air to get trapped in the alveoli. This trapped air makes breathing harder.

Over time, the air sacs lose their clustered shape and don’t work well. And less oxygen gets into the blood.

The air sacs get larger. This makes it even harder for the lungs to move air in and out.

Online Medical Reviewer:
Alan J Blaivas DO

Online Medical Reviewer:
Daphne Pierce-Smith RN MSN CCRC

Online Medical Reviewer:
Wanda Taylor RN PhD

Date Last Reviewed:
8/1/2018

Emphysema of the lungs

In 1826. Laennec,
watching a lung disease that
accompanied by their expansion and
an increase in airiness, called it
emphysema (from the Greek Emphesao
– I blow it up.)

Emphysema takes
one of the first places among diseases
lungs.

Secondary –
preceded by bronchitis with obstruction
bronchus

Acute obstructive
reversible. Observed when suffocating,
drowning, aspiration of loose substances,
during an attack of bronchial asthma.
Chronic
emphysema – most common in practice:

but. chronic
diffuse

b. chronic
focal

There are two main
emphysema type:

1.centrilobular
(centriacinar) and

2.panlobular
(panacinous).

Centrilobular
emphysema occurs with loss of airways
bronchioles in the proximal part of the acinus,
with preservation of the distal alveoli.
First of all, the upper lobes are affected.This option is most typical for
smokers.

Panacinar
emphysema occurs with the loss of all
parts of the acinus from the respiratory bronchiole
to the alveoli. The lungs reach the huge
sizes, often close the heart.
This option is typical for failure
α ₁ -antitrypsin.

Pathological anatomy Chronic diffuse obstructive emphysema

Macro:
in the section, the lungs are gray. Over
the incision surface is often
bronchi and blood vessels.The lungs are swollen.
go for each other. Increased.
Fluffy. Cut with a crunch.

May meet
pleural adhesions. From the bronchi it is excreted
mucopurulent plugs.

Micro:

atrophy
interalveolar partitions
coarsening
elastic frame
peribronchial,
interlobular sclerosis
hypertrophy
end plates
capillary reduction
channels

Bronchial asthma

Bronchial
asthma (from
Greek asthma
– choking) is a lung disease that
characterized by increased excitability
bronchial tree, which manifests itself
paroxysmal narrowing of the lumen
airways that are allowed
spontaneously or under the influence of medicinal
substances. Asthma is widespread
in the world, but the cause of death is
seldom. There are five main clinical
types of asthma:

atopic;
non-atopic;
induced
aspirin;
professional;
allergic
bronchopulmonary aspergillosis.

Each type has
various predisposing factors.
However, clinical signs for all
types are similar.

Atopic
asthma .
Atopic asthma is characterized by
the occurrence of seizures upon inhalation
various substances. Allergens can
be dust, pollen, food
products, excreta and animal hair.
Usually this type of asthma is
hereditary. These patients may
develop other types of allergic
reactions such as hay fever and
eczema.

Bronchospasm
arises from reactions
type I hypersensitivity. Mediators
bronchospasm, increased vascular
permeability and hypersecretion of mucus
are histamine and slow-reacting
substance of anaphylaxis (MRS-A). IN
as a result of the release of anaphylactic
eosinophil chemotaxis factor (ECF-A)
accumulates in the bronchial wall
a large number of eosinophils. Sometimes
the attack can be delayed, then
talk about status asthmaticus.

As a result
complex mechanism of reactions occur
the following pathological changes:

narrowing of the bronchi,
which leads to atelectasis or, conversely,
overflow of the alveoli with air;
blockage of the bronchi
viscous sputum;
inflammation of the bronchi;
the appearance of spirals
Kurshmana: spirals from desquamated epithelium
and phlegm;
the appearance of crystals
Charcot-Leiden: crystals in aggregates
eosinophils;
hypertrophy
mucous glands;
hypertrophy
smooth muscle tissue of the bronchi;
thickening of the basal
membranes.

Inflammation of
bronchi can spread to
bronchioles, which leads to local
obstruction, what is the cause
development of centrilobular emphysema.

Non-atopic
asthma . This
type is usually observed in patients with
chronic bronchitis. Mechanism
bronchoconstriction is not immune.
Skin tests for allergens are negative.
Bronchoconstriction presumably
arises from local
irritation of the bronchi with increased
reactivity.

Induced
aspirin asthma .
Patients with this type of asthma often
chronic rhinitis with polyps occurs
and skin rashes. Mechanism to the end
not clarified, but may be relevant
decreased production of prostaglandins and
increased secretion of leukotrienes, which
leads to increased reactivity.

Professional
asthma .
Occupational asthma occurs in
as a result of hypersensitivity to
certain substances inhaled on
work. These substances can be
nonspecific (act on non-immune
mechanisms on the bronchi with increased
sensitivity) or specific
(act by immune mechanisms with
the development of hypersensitivity I or / and
III type).

Allergic
bronchopulmonary aspergillosis .
Allergic bronchopulmonary aspergillosis
manifested by asthma, the cause of which
is constant inhalation of spores
mushroom Aspergillus
fumigatus , in
resulting in the development
type I hypersensitivity, and later
– Type III. Mucous plugs in the bronchi
contain aspergillus hyphae.

Pathological
anatomy .
Changes in the bronchi and lungs with bronchial
asthma can be acute, developing
at the time of the attack, and chronic,
resulting from repeated
attacks and prolonged course of the disease.

In the acute period
(during an attack) bronchial asthma
in the wall of the bronchi there is a sharp
plethora of blood vessels of the microcirculatory
channels and increasing their permeability.
Swelling of the mucous membrane develops and
submucosal layer, their infiltration
mast cells, basophils, eosinophils,
lymphoid, plasma cells.
The basement membrane of the bronchi thickens,
swells. Hypersecretion is noted
mucus goblet cells and mucous membranes
glands. In the lumen of the bronchi of all
calibers accumulate layered appearance
mucous secretion mixed with eosinophils
and cells of desquamated epithelium, obturating
the lumen of the small bronchi.At
immunohistochemical study
luminescence of IgE on the surface is detected
cells infiltrating the mucosa
the shell of the bronchi, as well as on the basal
membrane of the mucous membrane. As a result
allergic inflammation is created
functional and mechanical obstruction
respiratory tract with impaired drainage
functions of the bronchi and their patency. IN
lung tissue develops acute
obstructive emphysema, appear
foci of atelectasis, respiratory
failure, which can lead to
death of the patient during an attack
bronchial asthma.With repetitive
attacks of bronchial asthma with the course
time in the wall of the bronchi develop
diffuse chronic inflammation,
thickening and hyalinosis of the basement membrane,
sclerosis of interalveolar septa,
chronic obstructive emphysema
lungs. Desolation occurs
capillary bed, a secondary
hypertension of the pulmonary circulation,
leading to right heart hypertrophy
and ultimately – to the cardiopulmonary
failure.

Lobar emphysema of the lower lobe of the left lung

Congenital lobar emphysema (CLE) is a malformation characterized by emphysematous stretching of the parenchyma of the lobe or segment of the lung due to impaired development of the cartilaginous structures of the bronchus of the affected lobe [1-10].Other causes of lobar emphysema can be compression of the bronchus from the outside by cystic formations or abnormally located vessels, partial violation of bronchial patency due to hyperplasia of the bronchial mucosa or mucous plugs [1-5].

The clinical picture of the disease was first described in detail in 1951 by R. Robertson, and E. Jazmes called it lobar emphysema [4, 5].

Based on X-ray data and the severity of clinical manifestations, it is customary to distinguish between decompensated, subcompensated and compensated stages of the disease [2-5].Subcompensated and decompensated stages are found in newborns and children in the first months of life, at these stages the syndrome of intrathoracic tension is most pronounced. The compensated stage is observed in older children and is clinically similar to other lung diseases [4, 5].

With a compensated stage of VLE, clinical manifestations are very scarce. With a small degree of emphysematous enlargement, the disease is often detected by chance during X-ray examination at an older age [5].The incidence of VLE in children is 0.2% among acute lung diseases and 6.9% among lung malformations [3-5]. It was noted that VLE in 65% of cases is combined with other malformations: hypoplasia of segments, sequestration of the lung, arteriovenous aneurysm, anomalies in the development of the cardiovascular system, kidneys, intestines, musculoskeletal system [3-5].

According to the literature, VLE is more common in the upper lobe of the left lung – in about 60% of cases. However, it is often localized in the upper or middle lobe of the right lung, and cases of its detection in the lower lobe are quite casuistic.

We observed a child with lobar emphysema of the lower lobe of the left lung.

Patient T. , 13 years old, was admitted to the children’s department of thoracoabdominal surgery of the National Medical Center of the Republic of Tajikistan on December 10, 2013 with a presumptive diagnosis of a foreign body of the respiratory tract. From the anamnesis, it turned out that the child had been ill from birth and had been receiving outpatient treatment in various medical institutions for chronic pneumonia for a long time. At the next chest x-ray, a foreign body of the respiratory tract is suspected.

Upon admission, the patient’s condition is satisfactory. When examining the chest, there is an asymmetry of the chest in the form of a bulging on the left with an increase in intercostal spaces (Fig. 1) . On auscultation, vesicular breathing is heard over the right lung, and weakened breathing is heard on the left along the front and back of the chest. Indicators of blood and urine tests correspond to the age norm. On the roentgenogram of the chest organs in the projection of the upper lobe of the left lung, there is an increase in the airiness of the pulmonary fields, a pronounced depletion of the pulmonary pattern, displacement of the mediastinal organs in the opposite direction, flattening and low standing of the dome of the diaphragm on the affected side (Fig.2) . Computed tomography of the chest organs showed signs of lobar emphysema of the upper lobe of the left lung. The symptom of intrathoracic tension with displacement of the mediastinal organs to the right is determined (Fig. 3) . Diagnosed with congenital lobar emphysema of the upper lobe of the left lung.

An operation was performed as planned on 17.12. After thoracotomy on the left, it was found that the upper lobe was collapsed and displaced towards the mediastinal pleura, the lower lobe was emphysematous dilated, did not collapse during exhalation and occupied the entire pleural cavity.The interlobar gap is well expressed. The vessels of the lower lobe were isolated, stitched and tied. The bronchus of the lower lobe is crossed and sutured. The share has been deleted. The upper lobe of the lung is expanded. The pleural cavity is flushed and drained.

Morphological examination of the preparation revealed an emphysematous altered lower lobe.

Pleural drainage was removed on the 6th day after the operation, after which hemothorax occurred (Fig. 4, a) . The complication was eliminated with the help of pleural puncture.Hemostatic and symptomatic therapy was carried out.

On X-ray, the left pulmonary field is reduced in volume, pneumatized. Focal shadows are not detected. The roots of the lungs are structural. The shadow of the mediastinum is not enlarged. Free sinuses (see Fig. 4, b) The patient was discharged in satisfactory condition on the 16th day after the operation.

The difficulty in diagnosing VLE is associated with the scarcity and non-specificity of the clinical manifestations of the disease. In our observation, VLE of the lower lobe of the left lung was an intraoperative finding.Based on the examination data of this patient (X-ray and CT of the chest organs), the presence of VLE in the upper lobe of the left lung was suggested. The difficulty of diagnosing such a disease is determined by the rarity of the malformation.

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Pathological service: principles of organization, structure, tasks. Interaction with health authorities.The structure of the pathology bureau, the pathology department.
Pathological anatomy, content, tasks, objects, research methods. Clinical and anatomical direction of pathological anatomy.
Modern methods of morphological research.
Necrosis. Apoptosis. Definition. Morphogenesis of necrosis. Microscopic signs of cell necrosis, intercellular substance. Apoptosis, morphology, biological essence. Direct and indirect necrosis.
Clinical and morphological forms of necrosis. Coagulation and colliquation necrosis. Morphology of gangrene. Sequestration. Outcomes.
Heart attack. Definition. Types of infarction, morphology. The reasons for the development of a heart attack. Morphological features of the development of a heart attack in the heart, brain, kidneys, lungs, spleen. Outcome and significance of a heart attack.
Dystrophies. Definition of the concept. Classification. The reasons for the development of dystrophies. Morphogenesis of dystrophies. Types and essence of parenchymal protein dystrophies.
Fatty dystrophies. Histochemical stains for fat. Pathomorphology of myocardial fatty degeneration. Pathomorphology of fatty degeneration of the liver. Outcome and meaning.
Stromal-vascular dystrophies. Mucoid and fibrinoid swelling. Hyaline changes. Hyaline changes in various pathological conditions.
Amyloidosis. The essence of amyloidosis. Amyloid composition. Classification, causes of development. Histochemical reactions to amyloid. The morphological picture of the spleen.Changes in the liver, kidneys and other organs.
Stromal-vascular fatty degeneration. Impaired metabolism of neutral fats. Classification. Morphological changes in obesity. Causes and mechanism of development of general obesity. Meaning, outcomes.
Disorders of pigment metabolism, classification. Hemoglobinogenic pigments, types. Examples of general hemosiderosis. Examples of local hemosiderosis. The concept of hemochromatosis, its types.
Disorder of bilirubin metabolism.Lipidogenic pigments. Stages of bilirubin transport. Jaundice, types. The mechanism of suprahepatic jaundice. The mechanism of hepatic and subhepatic jaundice. Characterization of lipidogenic pigments.
Disorders of proteinogenic (tyrosinogenic) pigments metabolism. Melanin characteristics, melanogenesis. General disorders of melanin metabolism. Local disorders of melanin metabolism.
Disorders of nucleoprotein metabolism. The nature of nucleoproteins. Morphology of gout. Urolithiasis, uric acid infarction.The reasons for the violation of the metabolism of nucleoproteins. Outcomes.
Disorders of mineral metabolism. Morphology and causes of metastatic calcification. Dystrophic calcification, morphology, causes. Metabolic calcification, morphology, causes.
Circulatory disorders. Types of circulatory disorders. Definition of arterial plethora. Types of pathological arterial hyperemia. Characteristics of angioedema, collateral hyperemia. Hyperemia after anemia, vacate hyperemia.
Venous congestion. Definition of the concept. Views. The reasons for the development. Morphology of general and local acute venous plethora.
Chronic general venous congestion. The reasons for the development. Morphological processes arising during the development of general chronic venous stasis. Changes in the liver, lungs, kidneys, spleen in chronic venous stasis. Outcomes.
Anemia. Definition of the concept. Types of anemia. The morphology of acute and chronic anemia.Stasis. Definition of the concept. The meaning of stasis. Sludge phenomenon.
Thrombosis. Definition of the concept, reason. The mechanism of development of thrombus formation. Types of blood clots. Blood clot morphology. The difference between a blood clot and a postmortem blood clot.
Thrombosis. Pathogenesis and morphogenesis of thrombosis. Outcomes of thrombosis. The value of thrombosis. Definition, causes and mechanism of development of disseminated intravascular coagulation. Morphological manifestations of disseminated intravascular coagulation.
Embolism. Definition of embolism. Ways of movement of emboli.Types of embolism. Characteristics of fat, air and gas embolism. Tissue embolism.
Thromboembolism. Pulmonary embolism. Sources and causes of pulmonary embolism. Outcomes Thromboembolic syndrome. Sources, manifestations and outcomes.
Bleeding, hemorrhage. Definition of concepts. Types of bleeding. Causes and mechanism of bleeding. Shock, definition of the concept, types of shock. Pathomorphology of shock.
Inflammation.Definition. The biological nature and causes of inflammation. Classification. Pathogenesis and morphogenesis.
Fibrinous inflammation. The morphology of croupous inflammation, examples. The morphology of diphtheria inflammation, examples. Outcomes.
Purulent inflammation. Types of purulent inflammation. The course and outcome of purulent inflammation. Hemorrhagic inflammation. Catarrh.
Proliferative (productive) inflammation. Definition. Views. Interstitial inflammation.Granulomatous inflammation, causes, morphogenesis of granulomas.
Specific inflammation. Definition, its difference from commonplace inflammation. Morphology of tuberculous granuloma, gum. Leprosy granuloma. Scleroma granuloma.
Immunopathological processes. Changes in the thymus and changes in lymphoid tissue with disorders of immunogenesis. Pathomorphology of hypersensitivity reactions. Autoimmune diseases. The concept of immunodeficiency syndromes.
Regeneration.Definition. Regeneration levels. Morphogenesis of the regeneration process. Physiological and reparative regeneration. Pathological regeneration.
Atrophy. Process definition. Types of atrophy. General atrophy. Types of local atrophy. Outcomes and implications for the body.
Hypertrophy. Hyperplasia. Definition. Types of hypertrophy. Examples of hyperplasia. Hypertrophy of the heart, the reasons for its development. Morphology of compensation and decompensation of the heart.
Tumors. Definition of a tumor.The essence of tumor growth. Obligate precancer, facultative precancer (examples). Histogenetic classification of tumors. Tumor progression. Types of tumor growth.
Signs of a benign tumor. Signs of a malignant tumor. Metastasis. The concept of tumor recurrence. The effect of a tumor on the body.
Benign and malignant epithelial tumors without specific localization. Classification. Morphology.
Benign and malignant tumors from mesenchymal tissue.Histogenesis of mesenchymal tumors.
Tumors of melanin-forming tissue. Tumors of the nervous tissue and meninges.
Atherosclerosis. Definition of disease. Etiology of atherosclerosis. Macroscopic types of atherosclerotic changes. Stages of atherosclerosis morphogenesis. Signs of a wavy course and progression of atherosclerosis.
Atherosclerosis. Typical complications of atherosclerosis. Atherosclerosis of the aorta, types of aneurysms. Atherosclerosis of the vessels of the brain.Atherosclerosis of the renal arteries. Atherosclerosis of bowel vessels, lower extremities.
Hypertension. Definition. The concept of symptomatic hypertension. The pathogenesis of hypertension. Morphological characteristics of the stages of the disease, vascular changes. Clinical and morphological forms of the disease. Organ changes. Causes of death.
Ischemic heart disease. Definition, etiology and pathogenesis, risk factors. Ischemic myocardial dystrophy. Acute myocardial infarction, morphology.Complications of myocardial infarction.
Chronic ischemic heart disease. Definition. Myocardial infarction healing morphology. Cardiosclerosis. Chronic aneurysm of the heart. Causes of death of patients with coronary artery disease.
Rheumatism. Morphology of endocardial lesions, types of endocarditis. Rheumatic myocarditis, forms. Rheumatic pericarditis. Clinical and anatomical forms of rheumatism.
Rheumatoid arthritis. Etiology and pathogenesis, changes in the periarticular connective tissue.Stages and morphology of rheumatoid arthritis.
Acute bronchitis – etiology, pathogenesis and pathological anatomy. Definition of bronchopneumonia, etiology and pathogenesis. Pathological anatomy of bronchopneumonia. Morphological features of bronchopneumonia depending on the infectious agent. Legionnaires’ disease.
Croupous pneumonia. Definition, etiology and pathogenesis. Pathological anatomy of the stages of the disease. General manifestations of lobar pneumonia. Pulmonary complications. Extrapulmonary complications.
Chronic diffuse lung diseases. Chronical bronchitis. Bronchiectasis, developmental mechanism. Bronchiectasis, pathomorphology. Pneumofibrosis.
Emphysema of the lungs. Definition. Etiology and pathogenesis. Classification. Pathological anatomy of emphysema. Pulmonary heart, causes and mechanisms of development, morphology.
Lung cancer. Precancerous conditions. Classification. Pathogenesis and morphogenesis of central and peripheral lung cancer. Microscopic types.Complications of lung cancer.
Primary tuberculosis. Definition, etiology, pathogenesis. Morphology of the primary tuberculous complex in the lungs. Healing of the primary complex. Forms of progression of primary tuberculosis.
Secondary tuberculosis. Definition, distinctive features. Pathogenesis, forms. Acute focal tuberculosis. Fibrous focal tuberculosis. Infiltrative tuberculosis.
Secondary tuberculosis. Tuberculoma. Caseous pneumonia. Pathomorphology of fibro-cavernous tuberculosis.The structure of the wall of an acute and chronic cavity. The morphology of cirrhotic tuberculosis.
Viral diseases. Flu. Features of a viral infection. The relationship of the virus with the target cell. Influenza – etiology, pathogenesis. Pathomorphology of forms of influenza.
HIV infection. Etiology and pathogenesis. Periods, their clinical and morphological characteristics. Causes of death of patients with AIDS.
Measles. Definition. Etiology and pathogenesis. Enanthema. Exanthema. Complications.
Syphilis. Etiology and pathogenesis. Pathological anatomy of primary syphilis. Pathomorphology of secondary syphilis. Pathomorphology of tertiary syphilis. Visceral syphilis.
Diphtheria. Definition. Etiology and pathogenesis. Pathomorphology of local changes. Morphology of general toxic changes. Complications and causes of death.
Meningococcal infection. Etiology and pathogenesis. Classification. The role of immune complexes in pathogenesis. Pathomorphology of the main forms.Complications.
Typhoid fever. Etiology, pathogenesis. Local changes in the intestines. Pathomorphology of the stages of the disease. General changes. Complications of typhoid fever.
Dysentery. Etiology. Epidemiology and pathogenesis. Pathological anatomy of the stages of dysentery. Complications.
Sepsis. Definition, features of the infection. Pathogenesis. Pathological changes are local, general. Classification. Morphology of septicemia and septicopyemia.
Gastritis. Etiology and pathogenesis.Forms of acute gastritis, morphology. Classification of chronic gastritis. The morphology of chronic superficial and atrophic gastritis. Complications. Outcomes.
Peptic ulcer of the stomach and duodenum. Definition. Etiology and pathogenesis. Acute stomach ulcers. The morphology of a chronic ulcer in the period of exacerbation, healing. Complications of peptic ulcer disease.
Stomach cancer. Precancerous conditions. Classification. Histological types. Pathological anatomy.Regularities of metastasis.
Appendicitis. Definition. Morphological forms of acute appendicitis. Pathological anatomy of forms of acute appendicitis. Definition of the morphology of chronic appendicitis. Complications of acute and chronic appendicitis.
General characteristics of liver diseases, definition of hepatosis. Massive progressive liver necrosis, etiology, pathogenesis, pathological anatomy, outcomes. Fatty hepatosis, etiology and pathogenesis, pathological anatomy, outcomes.
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Cirrhosis of the liver. Definition, etiology. Morphogenesis. Morphogenetic types of liver cirrhosis. Pathological anatomy of cirrhosis. Complications. Liver cancer.
Glomerulonephritis. Definition of disease. Etiology and pathogenesis. Topography of inflammation in the glomeruli. Pathomorphology of acute and subacute glomerulonephritis. Chronic glomerulonephritis, morphology of its types.
Nephrotic syndrome – definition, classification. Lipoid nephrosis, membranous nephropathy, focal segmental glomerular sclerosis. Amyloidosis of the kidneys. Complications. Extrarenal changes.
Tubulopathy. Necrotizing nephrosis. Acute renal failure.
Interstitial nephritis. Pyelonephritis. Definition. Etiology. Pathogenesis. Pathomorphology of acute and chronic pyelonephritis. Complications, outcome.
Nephrosclerosis.Definition, etiology, classification. Pathological anatomy of nephrosclerosis. Definition of chronic renal failure. Pathological anatomy of uremia. Kidney tumors.
Diseases of pregnancy and the postpartum period. The concept of gestosis, etiology and pathogenesis. Eclampsia, pathomorphology. Ectopic pregnancy, spontaneous abortion. Bubble drift.
Diseases of the mammary glands. Fibrocystic disease. Diseases of the cervix and the body of the uterus.
Breast cancer.Precancerous conditions. Macroscopic characteristics. Histological types. Cancer of Paget. Metastasis.
Uterine cancer. Precancerous conditions. Cervical cancer. Histological types of cervical cancer. Cancer of the body of the uterus. Complications, metastasis.
Goiter (struma) – micro- and macroscopic species. Endemic and sporadic goiter. Diffuse toxic goiter (Basedow’s disease) – pathomorphology. Thyroiditis. Addison’s disease. Tumors of the endocrine glands.
Diabetes mellitus.Definition. Classification. Etiology and pathogenesis. Pathological anatomy of diabetes mellitus, angiopathy. Kidney damage in diabetes. Complications of diabetes mellitus.
The concept of nosology. Nosological unit. Nomenclature and principles of classification of diseases. International Statistical Classification of Diseases and Related Health Problems (ICD-X).
International histological classifications of tumors. Classification of the stages of the anatomical spread of malignant tumors (TNM system).
Lifetime pathological and anatomical studies. Biopsy concept, types of biopsy. Subject and conditions of intravital pathological and anatomical research.
Rules for taking, preserving and sending biopsy (operational) material for intravital pathological and anatomical examination.
Requirements for the design of Directions for intravital pathological and anatomical research.
Tasks and stages of the intravital pathological and anatomical study of biopsy (operational) material.
Terms and rules for filling out the Protocol of intravital pathological and anatomical research of biopsy (operational) material and its issuance.
Thanatology. Diagnosis, definition, its types.
The structure of the final clinical and pathoanatomical diagnoses.
Requirements for the formulation and coding of the final clinical and pathological anatomical diagnoses.
The underlying disease. Definition and characterization.
Complications of the underlying disease. Definition and characterization.
Concomitant diseases. Definition and characterization.
The concept of the original and immediate cause of death.
Monocausal diagnosis. Comorbism. Diagnosis formulation for comorbism.
Statement of biological death, transportation, procedure for receiving and storing corpses, issuing the body of the deceased.
Deontological aspects of the work of a pathologist.
The procedure for conducting pathological autopsies.
Autopsy protocol, structure and rules of execution.
Clinical and morphological comparisons.

Emphysema anatomy: Emphysema – Physiopedia

Emphysema – Physiopedia

Physiotherapy and Other Management[edit | edit source]

Emphysema – Physiopedia

Physiotherapy and Other Management[edit | edit source]

Emphysema – Physiopedia

Physiotherapy and Other Management[edit | edit source]

3. Anatomy and Physiology of Breathing

Anatomy of the Lungs

Physiology of Breathing

Obstructive and Restrictive Lung Disease

Effects of Smoking

Emphysema – StatPearls – NCBI Bookshelf

Continuing Education Activity

Introduction

Etiology

Epidemiology

Pathophysiology

History and Physical

Evaluation

Treatment / Management

Differential Diagnosis

Prognosis

Complications

Consultations

Pearls and Other Issues

Enhancing Healthcare Team Outcomes

Continuing Education / Review Questions

Figure

Figure

Figure

Figure

References

Pathology Outlines – Emphysema

What Is Emphysema?

Healthy lungs

When you have emphysema

Emphysema of the lungs

Pathological anatomy Chronic diffuse obstructive emphysema

Bronchial asthma

Lobar emphysema of the lower lobe of the left lung

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