I. Chronic bronchitis
It is a chronic non-specific inflammatory disease occurring in the bronchial mucosa and its surrounding tissues. The diagnostic criteria are: recurrent episodes of cough, sputum or with wheezing symptoms, and the symptoms persist for more than three months per year, with more than two years of continuous onset.
Etiology.
1, viral and bacterial infections; smoking; air pollution and allergies; intrinsic factors of the organism
2, pathological changes epithelial cell cilia adhesion, inversion, shedding, cell watery degeneration necrosis, increased cup cells, appear squamous.
3.Glandular hyperplasia and hypertrophy, mucus glands more than plasma glands, secrete a lot of mucus.
4, duct wall congestion edema, lymphocytes, plasma cell infiltration
5, smooth muscle fracture and atrophy (wheezing type hyperplasia hypertrophy), cartilage degeneration, atrophy, ossification. The lumen of the duct is irregular.
Eventually the wall is fibrotic and thickened, the lumen is narrowed or even atretic, and it is easy to expand to the tissue around the wall to form peribronchitis. The lesion spreads from the large bronchi to the small bronchi.
Clinical pathology is associated with coughing up white mucus-foamy sputum and acute attacks of coughing up mucopurulent or purulent sputum. Spasm or narrowing of the bronchi and obstruction of the lumen by mucus and exudate lead to wheezing.
Outcome: recovery; acute exacerbation (with acute purulent bronchitis); secondary emphysema, pulmonary heart disease; complication of bronchiectasis.
Second, bronchial asthma
Asthma is characterized by reversible episodic bronchial spasms caused by respiratory allergies. It manifests as recurrent episodes of expiratory dyspnea with croup, cough, chest tightness, etc.
Etiology.
Allergens, allergic constitution.
Pathological changes The lungs are distended by hyperinflation, soft and elastic, and the bronchial walls are thickened. The submucosal basement membrane is significantly thickened and vitreous, the fine bronchial smooth muscle is hyperplastic and hypertrophic, the walls are thickened, and the lumen is infiltrated with mucus plugs, cupped cells and mucus glands, eosinophilic c, mononuclear c, lymphatic c, and plasma c. Granules (disintegration products of eosinophils) and Curschmann spiral filaments (broken off epithelial cells and mucus) were seen in the duct wall and mucus plugs
Clinicopathologic linkage to exhalation dyspnea with croup due to fine bronchospasm and mucus embolism during an attack.
Complications: chronic bronchiectasis, bronchiectasis, emphysema, pulmonary heart disease
Bronchiectasis
Persistent dilatation of small bronchi in the lungs with fibrous thickening of the walls, with clinical manifestations of chronic cough, copious pus sputum, and recurrent hemoptysis.
Etiology.
Secondary to chronic bronchiectasis, etc.
Pathological changes often involve small and medium-sized bronchi below the segmental bronchi and larger than 2 mm in diameter. The bronchi are cylindrically or cystically dilated, with marked wall thickening, scaling, erosion, rough inner wall, mucopurulent or yellow-green purulent exudate in the lumen, numerous lymphocytic and plasma cell infiltrates, and atrophy, fibrosis or emphysema of the surrounding lung tissue.
Clinicopathologic association with frequent coughing, coughing up large amounts of pus sputum, and may hemoptysis leading to airway obstruction.
Complications: lung abscess, abscess chest, pneumothorax, pulmonary heart disease, etc.
IV. Emphysema
It is a common comorbidity of bronchial and pulmonary diseases due to excessive air content of terminal lung tissue with destruction of alveolar septum and decreased elasticity of lung tissue, resulting in enlarged lung volume and decreased function.
Etiology.
Obstructive ventilation disorders; decreased respiratory bronchial and alveolar elasticity; decreased alpha1-antitrypsin levels.
Types of alveolar emphysema: lesions occurring in the alveoli of the lungs, combined with obstructive ventilation disorders of the small airways, also known as obstructive emphysema.
They are divided into: central alveolar type – respiratory bronchial cystic dilatation
peri-alveolar – dilatation of the surrounding alveolar ducts and alveolar sacs
Total alveolar type – respiratory bronchi, alveolar ducts, and alveolar sacs. Alveoli are all dilated
Interstitial emphysema: mechanical injury causes a sharp increase in intrapulmonary pressure leading to rupture of fine bronchi or alveolar septa and entry of air into the interstitial lung. String-like bubbles appear in the lobular septa at the pleural junction.
Other types: paracranial, compensatory, senile
Pathological changes pale and less blood, increased volume, rounded edges, soft texture, poor elasticity, honeycomb-like cut surface, large pulmonary alveoli visible. Microscopically: enlarged alveoli, narrowed septa, enlarged interalveolar pores; septa mostly fractured and fused with each other; reduced capillaries, fibrous thickening of the intima of small arteries, resulting in pulmonary hypertension; chronic inflammation of the fine bronchi.
Clinicopathological link: dyspnea, shortness of breath, hypoxic manifestations. “Barrel-shaped chest”. Eventually leads to pulmonary heart disease.