What is the basic concept of silicosis and the basic molecular mechanism of its formation?

Silicosis is also known as silicosis.

It's pneumoconiosis. The most common type is the disease caused by long-term inhalation of large amounts of free silica dust, mainly extensive nodular fibrosis of the lungs. Silicosis is the most common, fastest-progressing, and most harmful type of pneumoconiosis.

There are about 20,000 new cases of pneumoconiosis in China every year. Therefore, the prevention and control of pneumoconiosis is a difficult task.

**。1.The concentration of dust in the air.

The higher the free SiO2 content in the environmental dust, the greater the dust concentration, the greater the harm caused. The dust concentration is expressed in mg m3, when the content of free SiO2 in the dust is large, and the concentration is very high (tens or even hundreds of mg m3), after long-term inhalation, silicon nodules are formed in the lung tissue.

2.Contact time.

The development of silicosis is a chronic process, usually occurring after 5 to 10 years of continuous inhalation of silica dust, and some for more than 5 to 20 years. However, continuous inhalation of dust with high concentration and high free silica content can cause disease after 1 to 2 years, which is called "immediate silicosis".

3.Dust dispersion.

Dispersion is a measure of the size of dust particles, expressed as a percentage of the composition of the various particle diameters in the dust. The greater the proportion of small particles, the greater the dispersion. The degree of dispersion is closely related to the fluctuation of dust particles in the air and their retention in the respiratory tract.

Dust particles with a diameter greater than 10um settle quickly in the air, and even if inhaled, they are blocked by nasal hairs and discharged with blowing nose; Most of the dust below 10um is blocked by the upper respiratory tract; Dust below 5um can enter the alveoli; The following dust, because of its small gravity, is not easy to settle, and is discharged with exhalation, so the retention rate decreases; However, the retention rate of the following dust increases due to Brownian motion.

4.Body status.

The human respiratory tract has a series of defense devices, and the inhaled dust, when it first passes through the nasal cavity, is blocked by the dust filter effect of the nasal hair and the curvature of the nasal septum, which is generally 30% to 50% of the amount of inhaled dust; Most of the dust entering the trachea and bronchi can be retained by the bifurcation of the bronchial tree and the movement of mucosal epithelial cilia and discharged with sputum; Some of the dust particles are macrophages.

or alveolar interstitial macrophages phagocytosis become dust cells, and dust cells or unengulfed free dust particles can travel along the lymphatic vessels into the hilar lymph nodes.

Those who have chronic respiratory tract inflammation have poor clearance function of the respiratory tract and respiratory system.

Infections, especially tuberculosis.

It can promote the rapid progression and exacerbation of the silicosis course. In addition, individual factors such as age, health quality, personal hygiene habits, and nutritional status are also important conditions affecting the onset of silicosis.

Basic concept: It refers to lung diseases characterized by the formation of silicon nodules and extensive pulmonary fibrosis caused by long-term inhalation of large amounts of free silica dust particles.

Basic molecular mechanism: The mechanism of silicosis has not been elucidated. Most scholars believe that after silica dust is engulfed by macrophages, the silica on the surface of silica dust reacts with water to form silicic acid, and its hydroxyl group forms hydrogen bonds with phospholipids in the secondary lysosomal membrane structure and hydrogen atoms in protein molecules, thereby changing the stability and integrity of the lysosomal membrane, enhancing the permeability of the membrane, causing macrophage lysosomes to disintegrate, and releasing a variety of proteolytic enzymes, causing the cell to disintegrate and die, and the silica dust is released, and it is engulfed by other macrophages, and so on.

Activated macrophages can release interleukins (IL), tumor necrosis factor (TNF), fibronectin (FN), etc., which can cause inflammation of lung tissue, promote fibroblast proliferation and collagen formation, macrophage proliferation and aggregation, and eventually lead to pulmonary fibrosis.

Dust is the most important occupational disease hazard factor leading to pneumoconiosis, dust is produced and present in many industrial production processes, the clinical manifestations of pneumoconiosis mainly include cough, sputum, chest pain, dyspnea four major symptoms, in addition to some patients can be combined with lung infection and tuberculosis, and produce some systemic symptoms.

There is no specific drug or method for pneumoconiosis, and the current clinical use of silicosis drugs can only reduce symptoms and delay the progression of the disease. At the same time as taking medication, we should actively treat the symptoms**, prevent complications, enhance nutrition, regularize life, and carry out appropriate physical exercise.

Silicosis: caused by long-term inhalation of a large amount of free silica dust, it is divided into: chronic silicosis, acute silicosis and rapidly progressive silicosis, among which chronic silicosis is the most common, mainly manifested as: cough, sputum production, chest tightness, shortness of breath, etc., which can be diagnosed by pulmonary function tests and X-ray chest X-ray.

The formation of silicosis is due to the dust in the breathing air, especially the silica component, after entering the alveoli, some are engulfed by lung cells, after the phagocytosis is fused with lysosomes, because the silica components are difficult to explain, they accumulate in the lysosomes, destroying the function of lysosomes, and many functions of the cells will also be affected, and the whole lung will show an abnormal state, thus forming silicosis.

After the silica particles in the air are inhaled into the alveoli, they are engulfed by the macrophages in the lungs to form phagosomes, which combine with primary lysosomes to form heterophagotic (secondary) lysosomes, silica particles cannot be degraded, silicic acid is formed on the surface of the particles in an acidic environment, and the hydroxyl group of silicate forms hydrogen bonds with the LY membrane or PR, resulting in the rupture of the LY membrane, the release of silica particles, and the phagocytosis of other macrophages, and so on, the macrophages continue to die, inducing fibroblasts to synthesize a large amount of collagen, This leads to the deposition of collagen fibers in the lungs and fibrosis of lung tissue, which reduces the elasticity of the lungs and reduces respiratory function.

Silicosis ()aThe partial pressure of oxygen in arteries is lower than normal.

b.The partial pressure of venous oxygen tolerance is higher than normal.

c.Arteriovenous oxygen levels are worse than normal.

d.Decreased oxygen volume deficit.

e.Arterial oxygen saturation is higher than normal.

Correct Answer: a

Correct answer: B

Analysis: The basic pathological changes in silicosis are silicone nodule formation and extensive pulmonary interstitial fibrosis.