Index
What is a Pulmonary Parenchyma?
Parenchymal lung diseases are disorders that affect the pulmonary interstitium. A surgical biopsy is the most accurate way to determine if a lung disease affects this part of the lung.
The term ” interstitial lung diseases ” has been replaced by “diffuse parenchymal lung diseases,” which means that the diseases appear to affect the lung areas around the air sacs on chest radiography and chest CT scans. However, some of them could affect other areas of the lung when a lung biopsy is performed.
All interstitial lung diseases affect the interstitium, a part of the anatomical structure of the lungs.
The interstitium is a network of lace-like tissue that spans both lungs. The interstitium supports the lungs’ microscopic air sacs (alveoli).
Small blood vessels travel through the interstitium, allowing the exchange of gases between the blood and the air in the lungs. Usually, the interstitium is so thin that it can not be seen on chest x-rays or CT scans.
There are hundreds of different types of diffuse parenchymal lung diseases, and the number is increasing rapidly as our ability to analyze these diseases continues to improve.
In general, it can occur due to one of the following causes:
- Infection
- Exposure to the environment
- Malignancy
- Occupational exposure
- Collagen vascular disease (an inflammatory disease of the body, including the lungs)
- Drugs
- Idiopathic (unknown cause)
Types of pulmonary parenchyma
All forms of pulmonary parenchyma cause thickening of the interstitium. The thickening may be due to inflammation, scarring, or extra fluid (edema). Some conditions of pulmonary parenchyma are short-lived; others are chronic and irreversible.
Some of the types of pulmonary parenchyma include:
Interstitial pneumonia: bacteria, viruses, or fungi can infect the interstitium of the lung. A bacteria called Mycoplasma pneumonia is the most common cause.
Idiopathic pulmonary fibrosis: a chronic and progressive form of interstitium fibrosis (scarring). Its cause is unknown.
Nonspecific interstitial pneumonitis: pulmonary parenchyma often presents with autoimmune conditions (such as rheumatoid arthritis or scleroderma).
Hypersensitivity pneumonitis: pulmonary parenchyma caused by the continuous inhalation of dust, mold, or other irritants.
Cryptogenic organized pneumonia: pulmonary parenchyma similar to pneumonia but without a present infection. Organized cryptogenic pneumonia is also called bronchiolitis obliterans with organized pneumonia (BOOP).
Acute interstitial pneumonitis: a sudden and severe pulmonary parenchyma that often requires life support.
Desquamative interstitial pneumonitis: pulmonary parenchyma caused partially by smoking.
Sarcoidosis: a condition that causes pulmonary parenchyma along with swollen lymph nodes and sometimes involvement of the heart, skin, nerves, or eyes.
Asbestosis: pulmonary parenchyma caused by exposure to asbestos.
Symptoms of pulmonary parenchyma
The most common symptom of all forms of pulmonary parenchyma is difficulty breathing. Almost all people with lung parenchyma will experience dyspnea, which may worsen over time.
Other symptoms of pulmonary parenchyma include:
- Usually dry cough.
- Weight loss, most often in people with organized cryptogenic pneumonia or BOOP.
In most forms of pulmonary parenchyma, difficulty breathing develops slowly (for months). In interstitial pneumonia or acute interstitial pneumonitis, symptoms appear more quickly (in hours or days).
The most common symptoms associated with diffuse pulmonary parenchymal diseases are shortness of breath and cough. Other symptoms may include fever, arthritis, weight loss, and rashes. Occasionally, a patient with diffuse parenchymal lung disease will have no symptoms, and the disease will be detected incidentally on a chest x-ray or a CT scan.
Causes
It is known that bacteria, viruses, and fungi cause interstitial pneumonia. Regular exposure to inhaled irritants at work or in hobbies can also cause lung parenchyma.
These irritants include:
- Asbestos.
- Silica powder.
- Talcum powder.
- Carbon dust or several other metallic powders from mining work.
- Grain powder from agriculture.
- Bird proteins (such as exotic birds, chickens, or pigeons).
Medications such as nitrofurantoin, amiodarone, bleomycin, and many others rarely cause pulmonary parenchyma.
In total, these factors cause a small percentage of lung parenchyma. The cause of most interstitial lung diseases is unknown.
Diagnosis
People with lung parenchyma usually go to the doctor due to shortness of breath or cough. Lung imaging tests are generally done to identify the problem.
Chest x-ray: a simple chest x-ray is the first test in the evaluation of most people with respiratory problems. Chest x-rays in people with pulmonary parenchyma can show fine lines in the lungs.
Computed tomography (CT) scan: A CT scanner takes multiple x-rays of the chest, and a computer creates detailed images of the lungs and surrounding structures. Lung parenchyma can usually be seen on a CT scan.
High resolution computed tomography: if there is suspicion of pulmonary parenchyma, certain adjustments of the CT scanner can improve the images of the interstitium. This increases the ability of the CT scanner to detect pulmonary parenchyma.
Pulmonary function test: a person sits in a sealed plastic cabinet and breathes through a tube.
People with pulmonary parenchyma may have reduced lung capacity. They may also have a lower ability to transfer oxygen from their lungs to the blood.
Lung biopsy: Often, the only way to determine what type of lung parenchyma a person has is to obtain lung tissue for examination under a microscope. There are several ways to collect lung tissue, which is called lung biopsy:
Bronchoscopy: An endoscope is advanced through the mouth or nose into the airways. Small tools in the endoscope can take a sample of lung tissue.
Video-assisted thoracoscopic surgery (VATS ): using tools inserted through small incisions, a surgeon can sample multiple areas of lung tissue.
Open lung biopsy (thoracotomy): In some cases, traditional surgery with a large incision in the chest is needed to obtain a lung biopsy.
Who is at risk for pulmonary parenchyma?
Anyone can develop pulmonary parenchyma. Men and women of any age can be affected. Lung parenchyma is more common in people with autoimmune diseases, such as lupus, rheumatoid arthritis, and scleroderma.
Treatments
Treatments for pulmonary parenchyma vary according to the type of lung parenchyma and its cause.
Antibiotics: These are effective treatments for most interstitial pneumonia.
Azithromycin and levofloxacin eliminate the bacteria that cause most interstitial pneumonia. Viral pneumonia usually resolves on its own.
Fungal pneumonia is rare but can be treated with antifungal medications.
Corticosteroids: In some forms of pulmonary parenchyma, continuous lung inflammation causes damage and scarring.
Corticosteroids such as prednisone and methylprednisolone reduce the activity of the immune system. This reduces the amount of inflammation in the lungs and the rest of the body.
Inhaled oxygen: in people with low oxygen levels in the blood due to pulmonary parenchyma, inhaled oxygen can improve symptoms.
Regular use of oxygen can also protect the heart from damage caused by low oxygen levels.
Lung transplant: A lung transplant may be the best option in advanced lung parenchyma that causes severe deterioration.
Most people who undergo lung transplantation for lung parenchyma make great strides in their quality of life and ability to exercise.
Azathioprine: This drug also suppresses the immune system. It has never been shown to improve pulmonary parenchyma, but some studies suggest it may be helpful.
N-acetylcysteine: this potent antioxidant may delay the decrease in lung function in some forms of pulmonary parenchyma. It should not be used alone.
Other treatments that are not used as often for pulmonary parenchyma include:
- Cyclophosphamide
- Methotrexate
- Cyclosporine.
- Pirfenidone.
- Nintedanib.
These medications significantly suppress the immune system. They can be used in some cases of interstitial lung disease while monitoring side effects.
Pathology in smokers
The earliest and most constant pathological abnormality in the respiratory tract is the cellular inflammatory infiltration through the wall.
Inflammation may be responsible for the slight limitation of the airflow. It has been suggested that inflammation can lead to functional bronchiolar constriction by releasing mediators that can act directly on the bronchiolar smooth muscle.
The chronicity of inflammation would, in turn, produce other changes, such as airway fibrosis, and could increase smooth muscle mass, either directly as a result of inflammation or indirectly as a result of chronically increased muscle tone.
By increasing the thickness of the airway wall, these changes would promote narrowing and limiting airflow. Inflammation of the respiratory tract may also play an essential role in forming pulmonary parenchyma.
The stimuli for this inflammatory infiltrate are not known with precision. Still, it is possible that the lesion of the airway epithelium, which is the first structure found by cigarette smoke, promotes and perpetuates the inflammation in the respiratory tract.
Epithelial cells have the potential to initiate airway inflammation through the metabolism of arachidonic acid. For example, a product of this route, dihydroxieicosatetraenoic acid, is a potent signal to recruit neutrophils to the respiratory tract.
Another system involved in the inflammatory responses of the respiratory tract, possibly triggered by the loss or alteration of the epithelial surface, is neurogenic inflammation.
Stimulation of the sensory nerves in the airway epithelium releases tachykinins, including substance P and neurokinins A and B. These tachykinins cause the chemotaxis and adhesion of neutrophils, stimulate the release of cytokines, and cause degranulation of the eosinophils.
In animal studies, exposure to cigarette smoke and other irritants promotes the rapid onset of neutrophils in the respiratory tract.
They also showed that when the mucosa of aerosolized tails is injured by inhaling cigarette smoke, edema forms in 30 min, and the number of neutrophils in the airway epithelium increased fivefold from the control values measured six h after the injury.
Not surprisingly, neutrophils are found abundantly in the walls of the respiratory tract of smokers, and the number of submucosal neutrophils correlates significantly with the dose of cigarette smoke.
However, at least in some reports, the number of neutrophils in the walls of the airways is no different in smokers with or without airflow obstruction.
These first inflammatory events in smokers may not be specific and represent an innate immune response to the airway injury.
Other irritants will also trigger an inflammatory reaction in the respiratory tract. For example, they reported that inhalation of acid in dogs caused abnormalities in the function of the small airways that were associated with an accumulation of neutrophils in the non-cartilage airways.
Similarly, the inhalation of NO 2 causes a rapid increase in airway resistance and the responsiveness of the airways with an influx of neutrophils followed by mononuclear cells.
Changes induced by SO 2 have also been described, consisting of a marked neutrophilic infiltration of the respiratory tract and an increase in resistance.
The inhalation of neutrophil elastase also causes increases in the total cell counts of the BAL fluid. It is accompanied by epithelial damage, mucus plugging, and infiltration of neutrophils and macrophages in the bronchial mucosa.
Ozone exposure has been extensively studied in human volunteers. It can describe events occurring in the airways after repeated exposure to a respiratory irritant ( p Eg. , NO 2, SO 2, ozone, cigarette, or gas).
Acute exposure to ozone leads to an increase in neutrophilic and mononuclear cells, increases total protein concentration, interleukin (IL) -6 and IL-8, and reduces glutathione levels in BAL fluid.
The earliest and most constant pathological abnormality in the respiratory tract of smokers is the cellular inflammatory infiltration through the wall.
Therefore, the “early” inflammatory infiltrate found in the respiratory tract of smokers and reflected in pulmonary function tests probably represents a nonspecific response of the respiratory tract to the lesion in general.
However, a significant difference between the insult of cigarette smoke and those described above may be the chronic inflammatory stimulus produced by the daily inhalation of cigarette smoke.
Therefore, it would seem that most smokers would develop chronic and nonspecific inflammation in the respiratory tract and lung parenchyma, but, for unknown reasons, some smokers develop severe airway abnormalities and emphysema, which eventually develop into Clinical COPD.
